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Reproduction Flashcards

1
Q

What are the classic signs of oestrous?

A

Female is stood to be mounted- sexually receptive to the male.

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2
Q

What is the fertile period?

A

The time, before and after, where insemination could result in a pregancy.

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3
Q

In what species is progesterone a measurable indicator of ovulation?

A

Dog

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4
Q

In what species is LH an indicator a measurable of ovulation?

A

Dogs and Cats

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5
Q

Why can an increase in progesterone be used to indicate ovulation in the dog?

A

The increase in P4 indicates luteinisation and thus immanent ovulation.

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6
Q

Why can LH be used to indicate ovulation?

A

The LH surge triggers ovulation.

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7
Q

You perform a rectal ultrasound on a cow:

There is an active CL, what does this mean with regards to optimum time to breed?

A

An active Cl means that P4 is high and therefore ovulation can not occur.

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8
Q

What size of a bovine follicle is likely to indicate immanent ovulation?

A

A follicle between 16-20mm.

A follicle will not ovulate if it is smaller than 10mm

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9
Q

What sized follicle would you introduce the stallion to the mare?

A

Typically between 35-50mm as this indicates that ovulation is likely.

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10
Q

What are you likely to note on rectal examination of a cow in oestrous?

A

That the cervix is narrow and tense. The uterus is oedematous with increased tone.

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11
Q

You rectal a cow and note that the: cervix is soft and flaccid, and the uterus is flaccid with reduced tone. Is oestrous likely, why?

A

No, as these clinical signs indicate that the cow is in the luteal phase, where progesterone is dominant.

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12
Q

You rectal a horse and note that the cervix is broad and soft, and the uterus is larger and more oedematous. Is this a good time to introduce the stallion, why?

A

Yes, as it indicates that they mare is in oestrous, where oestrogen is the dominant hormone. Therefore, ovulation is likely to occur.

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13
Q

What clinical signs would you expect to find when rectalling a horse in the luteal phase?

A

Cervix: hard and narrow
Uterus: smaller with increased tone
Because progesterone is dominant.

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14
Q

What is the key notifiable disaese in mares which relates to breeding?

A

Contagious equine metritis (CEM) - Notifiable

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15
Q

Upon clinical exam you note this on the mare:

What is this and what risks are associated with it?

A

Poor vulval conformation (sloping vulva). The vulva sits at an angle that is more likely to trap faeces and gas. This makes an acending infection more likely. Greater risk of (endo)metritis.

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16
Q

What are the optimum pregancy dignostic indicators of the cow, and at what day can they be done at?

A
  • Transrectal ultrasound - Day 28
  • Transrectal palpation - Day 35
  • Transrectal ballotment of foetus - Day 50
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17
Q

What are the optimum pregnancy diagnostic indicators of the ewe, and at what day can they be done at?

A
  • failure to be raddled - Day 16-19
  • Transabdominal ultrasound - Day 30
  • Foetal pulse detector with doppler ultrasound - From Day 80
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18
Q

What are the optimum pregnancy diagnostic indicators of the sow, and at what day can they be done at?

A
  • Failure to return to oestrus - day 18-24
  • Transabdominal B-mode ultrasound - from day 20
  • Elevated plasma progesterone - day 22-24
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19
Q

What are the optimum pregnancy diagnostic indicators of the mare, and at what day can they be done at?

A
  • Failure to return to oestrus - day 18-24
  • Transrectal ultrasound from day 12 (15 common)
  • Transrectal palpation from day 21
  • Plasma equine chorionic gonadotrophin from day 60 – 120
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20
Q

What are the optimum pregnancy diagnostic indicators of the bitch, and at what day can they be done at?

A
  • Transabdominal ultrasound - from day 25
  • Plasma relaxin - from day 25
  • Radiographic examination - from day 45
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21
Q

What are the optimum pregnancy diagnostic indicators of the queen, and at what day can they be done at?

A
  • Transabdominal ultrasound - from day 25
  • Plasma relaxin - from day 25
  • Radiographic examination - from day 45
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22
Q

What can not be used to diagnose pregnancy in the bitch?

A

A lack of return to oestrous

Elevated plasma progesterone.

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23
Q

What techniques may be used to examine the accessory glands?

A

– Semen collection
– Rectal palpation
– Radiographic (often including positive contrast)
– Trans-rectal or trans-abdominal ultrasonography
– Lavage techniques

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24
Q

What is the submission rate?

A

The percentage of cows served.

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25
Q

What is a true hermaphrodite?

A

The karyotype is more often
XX. Histological evidence of ovarian and testicular
tissue (E.g. ovotestis). Ambiguity of external or
internal genitalia or both.

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26
Q

What is a male pseudohermaphrodite

A

The karyotype is XY. The gonads are recognisable as testis. Incompletely masculinised and ambiguous external and internal genitalia

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27
Q

What is a female pseudohermaphrodite

A

The karyotype is XX. Feminine internal genitalia, masculinised external genitalia.

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28
Q

Outline a potential cause of epididimitis and why it is significant.

A

Brucella ovis - notafiable

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29
Q

What is conception failure?

A

The failure of fertilisation:
Mistiming of mating
Ovulation failure/delay
Male infertility

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30
Q

What is embryonic death?

A

Death after fertilisation

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31
Q

What species is early preganacy loss uncommon?

A

Cats, Dogs and Sheep

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32
Q

Ouline some cuases of failure to establish pregnancy in cows.

A

Conception failure assosiated with: metalbolic stress or ovaian pathology.

Failure to detect oestrous

Mis-timing of AI

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33
Q

Outline some of the causes of embryo mortality in cows?

A

Failure to secrete materal recognition hormone.

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34
Q

Outline some causes of failure to establish pregnancy in sows.

A

Seasonal affects- decreased in summer/autumn

Ovulation failure: stress/pathology

Genetics

Infectios causes: parvoviris (PPV)

Nutrition

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35
Q

Outline some causes of failure to establish pregnancy in mares.

A

Age of the horse

Haemorrhagic anovulatory follicles

Uterine pathology

Infectious causes: CEM

Stress

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36
Q

Outline the clinical use of GnRH.

A
  • As part of OvSynch
  • Hasten ovulation by inducing LH surge
  • Force ovulation/luteinisation of cyctic structures
  • Measure sex steroid response
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37
Q

Outline the long term clinical use of GnRH.

A
  • Initial stimulation, follwed by down reculation and thus supression of HPG axis.
  • Control/supress oestrous behaviour
  • Controls fertility in male dogs (prevents breeding)
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38
Q

Outline the clinical use of FSH/LH?

A

Induce superovulation

and other similar treatments to GnRH. They are used much less.

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39
Q

Outline the clinical use of progesterone.

A
  • Vaginal (PRID/Sponges): Induction of oestrous. Synchronisation upon withdrawal.
  • Depo: prevention of oestrous in bitches.
  • Oral: prevention/suppression of oestrous in bitches and prevention/induction/suppression in mares.
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40
Q

Outline the clinical use of a progesterone receptor antagonist.

A

Termination of pregnancy

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41
Q

Outline the clinical use of oestrogen.

A

Urinary incontinence in the bitch.

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42
Q

Outline the clinical uses of PGF2a

A
  • Termination of luteal phase to synchronise oestrus
    − Induction of abortion
    − Induction of parturition
    − Ecbolic effect (contractions)
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43
Q

Outline the clinical uses of prolactin inhibitors.

A
  • Removes support for CL (prolactin)
  • To end the luteal phase
  • Terminate pregnancy
  • Treat pyometra
  • Reduce milk production and behaviour of pseudopregancy
  • To reduce milk after weaning.
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44
Q

Outline the clinical uses of melatonin.

A

Hasten onset of cyclicity in sheep.

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45
Q

Outline the clinical uses of oxytocin.

A
  • Initiation of uterine conractions- to aid parturition.
  • Promotion of involution of post-parturient uterus
  • Aid passage of retained placenta
  • Promotion of milk let-down in agalactia
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46
Q

Outline the clinical use of GnRH/hCG in males.

A

For testing for presence of a testis.

Depot GnRH for suppression of HPO axis (reduce male behaviours)

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47
Q

Outline the clinical use of progesterone in males.

A

Reduction on testosterone production

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48
Q

Outline the OvSynch protocol

A

Day 0 - GnRH
Day 7 - PGF2a
Day 9 - GnRH
Day 10 - AI (16-20hrs later)

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49
Q

Outline the OvSynch with P4 protocol.

A

Day 0 - Insert PRID and inject GnRH
Day 7 - Remove PRID and inject PGF2a
Day 9 - GnRH and AI

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50
Q

In what type of animal would the OvSynch and P4 protocol be used

A

Cycling and non-cycling cows

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51
Q

Outline the P4 and PGF2a protocol

A

Day 0 - Insert PRID
Day 7 - Remove PRID and inject PGF2a
Day 10 - 1st AI
(Day 10.5 - If single AI only)
Day 11 - 2nd AI

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52
Q

State the clinical treatment of a cow in anovulatory anoestrus.

A

OvSynch with P4

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53
Q

Outline the clinical treatment for cyctic ovarian disease.

A

Follicular phase: GnRH/hCG

Luteal phase: PGF2a

OvSynch - Either!

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54
Q

Outline the clinical treatment for persistent CLs.

A

PGF2a

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55
Q

List the advantages of surgical nuterining in females.

A

– Reduction in the incidence of mammary neoplasia
– Prevention of uterine disease including CEH, pyometra and uterine neoplasia
– Prevention of ovarian disease including neoplasia
– Prevention of (pseudo)pregnancy

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56
Q

List the disadvantages of surgical nuterining in females.

A

– Increased incidence of some neoplasia (osteosarcoma, hemangiosarcoma)
* In some breeds there is a clear relation the longer that ovaries or testes are present the
lower this risk
– Increased incidence of urinary incontinence in dogs?
– Changes in coat texture?
– Tendency to gain weight?
– Changes in behaviour

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57
Q

Describe the best timing for female sterilisation.

A

3 months after oestrous or 3 weeks post oestrous.

Prevents pseudopregnancy

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58
Q

Outline the three types of female surgical nutering and which is the most common in the UK.

A
  • Ovariohysterectomy (UK most common)
  • Ovariectomy (Lap spays)
  • Hysterectomy
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59
Q

When should queens be spayed?

A

Anytime apart from oestrus as the tract is more vascular and friable.

60
Q

Outline the surgical techniques for castration

A

Open

Closed

Modified

61
Q

Outline the advantages and disadvantages of the open technique.

A

Rapid, effective observation of vasculature, allows good drainage, may be useful when conditions likely to be contaminated,

Herniation risk increased

62
Q

Outline the advantages and disadvantages of the closed technique.

A

Rapid, does not allow observation of vasculature but effective haemostasis if surgical
field controlled, peritoneal contamination minimised, herniation risk reduced

63
Q

Outline the advantages and disadvantages of the modified technique.

A

More time consuming, allows good haemostasis and surgical closure but only if surgical conditions are guaranteed clean, herniation risk reduced

64
Q

Outline the methods for castration of the cat

A
  • Open following twisting and traction
  • Open following ligation
  • Open following auto-ligation
65
Q

Outline castration options for the calf

A

Elastication (first 7 days)

Crushing

66
Q

Outline castration options for the bull.

A

Surgical (open)

Use of emasculators

67
Q

Outline castration methods for the pig.

A

Surgical - open, no ligature or emasculation.

68
Q

When is the optimum time for castration in the dog.

A

After 12 months

69
Q

Outline complications associated with surgical neutering.

A
  • Anaesthesia related
  • Bleeding
  • Damage to other organs
70
Q

Outline complications during the recovery associated with surgical neutering.

A
  • Anaesthesia related
  • Bleeding
  • Herniation of omentum in stallion
  • Eventration in the stallion
71
Q

Outline immidiate complications associated with surgical neutering.

A
  • Wound related problems (infection, breakdown etc)
  • Scrotal haematoma
72
Q

Outline long term complications associated with surgical neutering.

A
  • Surgical materials left inside animal
  • Pyogranuloma
  • Incomplete removal of the gonads
  • Incontinence in the bitch
  • Increased risk of other diesases
  • Body conformation changes
73
Q

Outline the anatomical causes of in/subfertility in females.

A

Congenital deformation

74
Q

Outline the physiological causes of in/subfertility in females.

A

Ovarian pathology

Uterine infection

Failure to establish pregnancy

75
Q

Outline the management causes of in/subfertility in females.

A

Nutrition

Oestrus detection

Genetics

Timing of mating

Expectations

Stress

76
Q

Define fertile

A

Capable of producing offspring

77
Q

Define sterile

A

Absolute inability to produce offspring

78
Q

Define infertility

A

a factor of the breeder’s expectations of the outcome following a mating

79
Q

Outline the abnormalities that affect male fertility.

A
  • Abnormalities of coitus
  • Failure of fertilisation
80
Q

Outline the common abnormalities of coitus

A

– Immaturity and inexperience
– Inability or unwillingness to mount
– Inability to achieve intromission
– Haemospermia

81
Q

Outline the common reasons for failure of fertilisation. (male)

A

– Testicular disease
– Sperm abnormalities (may be associated
with gross testicular or epididymal disease)
– Epididymal lesions
– Accessory gland disease

82
Q

Outline the common reasons for failure to achieve intromission.

A
  • Failure of erection
  • Penile deviations
  • Penile trauma
  • Preputial abnormalities
83
Q

Outline what happens if fetal death occurs at day 160 (cow).

A

Possible mumification as the CL is still active.

However, bateria/inflammation could cause the release of prostaglandin and cause abortion.

84
Q

Outline what would happen if fetal dealth occurs at day 260 (cow)?

A

Expulsion as there is no CL. The L-P shift occurs between days 210-250

85
Q

What would occur if embryonic death occured at day 80 (cow).

A

Reabsorption or possible pyometra. As fetal mineralisation does not occur until day 90.

86
Q

Outline the non-infectious causes of embryonic and fetal death.

A

– Genetic abnormalities
– Uterine disease (not able to form effective placenta)
– Stress (nutritional, heat, other)
– Maternal illness
– Nutritional phytotoxins

87
Q

When the L-P shift occur in the horse?

A

140-210 days

88
Q

When does the L-P shift occur in the cow?

A

210-250 days

89
Q

When the L-P shift occur in the sheep?

A

50 days

90
Q

What species do not have a L-P shift?

A

Dog, cat, pig, goat - the CL produces P4 the whole time, so any pregancy loss will be carried until parturition.

91
Q

What changes in endocrinology cause parturition?

A

Late term production of relaxin causes softening/dialation of cervix and ligaments.

Fetal maturation/stress casues an increase in PGF2 and a decrease in P4.

This stimulates the relsease of and lowers the threshold for effect of oxytocin which causes contractions

92
Q

Outline common reasons for dystocia.

A

Maternal:

  • Inadequate expulsive forces
  • Inadequate size of birthing canal.

Foetal:

  • Oversize
  • Fault disposition- presentation
93
Q

Outline common post-partum conditions.

A
  1. Haemorrhage
  2. Trauma/lacerations/contusions
  3. Prolapse of something
  4. Placental retention
  5. Metritis
  6. Recumbency / nerve damage
94
Q

Outline surgical treatments for dystocia.

A

– Epidural anaesthesia
– Episiotomy
– Fetotomy
– Caesarean operation

95
Q

Outline drug therapy for dystocia.

A

Oxytocin/PGF2a
Clenbuterol
Calcium

96
Q

Outline treatments for dystocia

A
  • Manipulation
  • Drugs
  • Surgical
  • Euthanasia
97
Q

What are the indications for a caesarean

A
  • The fetus cannot be delivered by mutation and traction
  • Dystocia is correctable but there is a large litter so risk of secondary inertia or dam exhaustion
  • There is uterine torsion or incomplete cervix dilation that
    cannot be remedied
  • When fetotomy would be extensive, traumatic and time
    consuming
  • Performed as an elective procedure where there is high risk.
98
Q

Outline the correct needle placement for a proximal paravertebral nerve block in cattle.

Local Anaesthetic for a c section

A

T13, L1 and L2 off to the side of the vertebra

99
Q

Name two conditions that neonates are at high risk of?

A

Hypovolaemia
Hypoglycaemia

100
Q

What antibodies does colostrum contain?

A

IgG (65-95%)

Rest: IgM and IgE

101
Q

Outline the causes of FPT

A

Poor quality colostrum

Poor intake of colostrum (quantity/time)

102
Q

Outline some common conditions assosicated with neonates.

A
  • FPT
  • Limb deformities
  • Hernias
  • sepsis
  • Diarrhoea
  • Bladder rupture
  • Colic
  • Pneumonia
103
Q

Outline common mammary disorders.

A
  • Diseases of the local skin or mammary skin
  • Damage of the udder suspensory apparatus (dropped udder)
  • Damage to the teat skin (e.g. milking machine trauma),
  • Damage to the teats
  • Inverted nipple
  • Skin disease
  • Mastitis
  • Enlargement
  • Neoplasia
  • Agalactia
104
Q

What does the TNM tumour grading system stand for?

A

T- primary tumour diameter
N- regional lymph nodes
M- Distant metastasis

105
Q

Explain what is meant by T1, T2 and T3 scores.

A

T1- Diameter less than 3cm

T2 - Diameter between 3-5cm

T3 - Diameter greater than 5cm

106
Q

What is meant by N0 and N1 scores.

A

N0 - No metastasis on histiopathology/cytology in the local nodes

N1 - Metastasis detected

107
Q

What is meant by M0 and M1 scores?

A

M0 - No distant metastasis.

N1- Distant metastasis detected.

108
Q

What would a mammary neoplasia score of T2, N1, M0 indicate

A

Tumour is 3-5cm, metastasis in local nodes but no distant spread.

109
Q

Grade the following mammary tumour:

A 6cm tumour, with spread to local nodes and to the lungs.

A

T3, N1, M1

110
Q

Outline the clinical treatment options for agalactia caused by failure of milk production.

A

Metoclopramide (prolactin agonist)

111
Q

Outline the clinical treatment options for agalactia caused by failure of milk letdown.

A

Oxytocin

112
Q

Outline the two upper urinary tract infections.

A

Pyelonephritis

Nephritis

113
Q

Outline the mechanisms for UTIs.

A

Descending infection (nephritis/polynephritis)

Or ascending from urethra

114
Q

Outline the common UTIs.

A

Ureteritis
Cystitis
Urethritis

115
Q

Outline the bacteria commonly involved in UTIs.

A

E. Coli
Proteus Vulgaris
Strep
Staph
Enterococci

116
Q

What is Amyloidosis?

A

Extracellular deposition of amyloid
(eosinophilic, homogeneous and proteinaceous material)

117
Q

Describe nephrotic syndrome

A

Prolonged, severe renal protein loss.

A collection of physiological signs that indicate impared renal function. These include: proteinuria (albuminuria), hypoproteinaemia
(hypoalbuminaemia), hyperlipidaemia, generalised oedema.

118
Q

How does nephrotic syndrome occur?

A

Damage to glomerular filtration barrier causes leak of low MW proteins into the filtrate. This exceeds the reabsorption capabilities, resulting in protein in the urine.

The decreased plasma protein levels reduce the plasma colloid pressure causing hypovolaemia. This triggers the RAAS system and release of ADH.

119
Q

Outline what glomerulonephritis is.

A

Inflammation of glomeruli with secondary tubulointerstitial and
vascular changes

120
Q

Outline common causes of glomerulonephritis

A
  • Deposition of immune complexes
  • Persistent antigenemia
  • Viral infections
  • Chronic bacterial infections
  • Chronic parasitism
  • Neoplasia
121
Q

Outline causes of tubular disease/necrosis

A

Hypoxia - reduced O2 to kidney, tubules die

Nephrotoxicity- drugs etc destroy tubules

122
Q

Outline the consequences of tubular disease.

A

Acute renal failure or chronic interstitial nephritis.

123
Q

Outline Tubulointerstitial nephritis and the main types.

A
  • Diseases involving primarily the interstitium and tubules
  • Main types:
    a. Suppurative
    b. Non-suppurative
124
Q

Outline what a patent urachus is and its likely complicatios.

A

A communication between
bladder and umbilicus that should have closed after birth.

Associated with :
- infection
- cysts and diverticulums
- Uroperitoneum in rare circumstances

125
Q

Outline differential diagnoses for umbilical swellings.

A
  • Persistent urachus
  • Abscess
  • Umbilical Hernia
126
Q

Outline the common causes of renal failure.

A
  • CKD
  • AKI
127
Q

What is AKI?

A

Sudden onset damage which might be:
* Reversible
* Progressive - permeant loss of nephrons.
* Rapidly fatal
* A complication

128
Q

Outline possible causes of AKI.

A
  • Poor renal perfusion (Cardiovascular disease)
  • Hypoxia
  • Nephrotoxins: NSAIDs, Vitamin D, grapes and anti-freeze
  • Obstructive disease
  • Infection
  • Hypercalcaemia
  • Alabama rot
129
Q

What is CKD?

A

Presence of functional or structural changes in 1 or both kidneys for
> 3 months

130
Q

Outline possible causes of CKD.

A
  • Consequence of AKI
  • Ischaemia
  • Inflammation
  • Auto-immune
  • Unknown
131
Q

What is ischaemia?

A

A reduction in perfusion/blood flow to a certain part of the body.

132
Q

Outline biochemistry results that would indicate AKI

A
  • Increased urea
  • Increased creatinine
  • Increased phosphoros
  • Increased potassium (due to decreased urine output)
  • Increased calcium
  • Decreased calcium (ethylene glycol toxicity)
133
Q

Outline biochemistry results that would indicate CKD

A
  • Increased urea
  • Increased creatinine
  • Increased phosphoros
  • Decreased potassium (due to increased urine output with polyuria)
  • Increased calcium
  • Decreased calcium (ethylene glycol toxicity)
134
Q

Outline urinalysis results for CKD and AKI.

A
  • Contextual USG
  • Glucose - tubular damage (AKI)
  • Protein
  • Blood
135
Q

Outline ureteric abnormalities.

A
  • Ectopic ureter
  • Traumatic injury to ureters
  • Ureteral obstruction
136
Q

Outline the causes of uroperitoneum

A
  • Ruptured bladder - most common
  • Urethral tears
  • Urachal rupture (neonates)
  • Bladder stones
  • Trauma
137
Q

Outline the clinical signs seen with uroperitoneum/ruptured bladder.

A
  • Neurological signs
  • Anuria/dribbling little urine
  • Straining to urinate
  • Abdominal distension
  • Tachycardia
138
Q

Outline the biochemistry markers for uroperitoneum/ruptured bladder.

A
  • Hyperkalaemia
  • Hyponatremia
  • Hypochloraemia
  • High creatinine
  • Metabolic acidosis
139
Q

Ouline the ultrasonographic apperance of uroperitoneum

A

Large amount of hypoechoic free peritoneal fluid

140
Q

Outline the markers seen on abdominocentesis.

A

Creatinine concentration at least 2 times that of blood.

141
Q

Outline the treatment of uroperitoneum/ruptured bladder.

A
  • Drain peritoneal cavity of fluid
  • Fluid therapy to correct electrolyte imbalances - isotonic saline with 5% glucose (+/- insulin)
  • Broad spectrum antimicrobials - enrofloxacin or cephalexin.
  • NSAIDs - carprofen, meloxicam
  • Surgical Repair of the bladder
  • Euthanasia
142
Q

Vaginal cytology is taken from a bitch. What stage of the cycle is she in? Why?

A

Anoestrous - as there are many parabasal and small intermediate cells.

143
Q

Vaginal cytology is taken from a bitch. What stage of the cycle is she in? Why?

A

Proestrus - as there are larger quantities of large intermediate (nucleated) cells and RBCs are present.

144
Q

Vaginal cytology is taken from a bitch. What stage of the cycle is she in? Why?

A

Oestrous - as there are now large numbers of anuclear cells, and no small intermediate cells. There are also fewer RBCs

Early oestrous would be similar, however, there would be fewer anuclear cells and more RBS and nucleated cells.

Look for - RBS and anuclear cells as this is oestrous!

145
Q

Vaginal cytology is taken from a bitch. What stage of the cycle is she in? Why?

A

Early metoestrous - as there are few RBCs, many WBCs (neutrophils), few anuclear cells, and increasing numbers of nucleated cells.

FCP (14 decks)

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