mcq 2 pcp Flashcards

1
Q

vsmall animal oestrus cycle

A

Pro-oestrous (10 days)
Oestrous (10 days)
Luteal phase (2 month)
Pregnant or non-pregnant
Anoestrous (4.5 months)

P4 from CL only
LH and prolactin luteotrophic

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2
Q

Average gestation in the bitch

A

63-64 days (range 56-72 days)
calculated either from
preovulatory surge of luteinizing hormone (LH) (65 ± 1 days)
day of ovulation (63 ± 1 days)
time of fertilization (60 ± 1 days)

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3
Q

principles of pregnancy diagnosis

A

Detection of protein / endocrinological changes associated with pregnancy

  1. Detection of the fetus or fetal membranes either directly or indirectly:
    Abdominal palpation
    Ultrasound examination
    Radiographic examination
  2. Detection of physical changes in the dam which are associated with her accommodating a fetus (increased size of the uterus)
  3. Detection of maternal changes that are secondary to endocrinological changes
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4
Q

Plasma Progesterone Concentration

A

No rapid return to oestrus
Not sufficiently different between pregnant and non-pregnant bitches

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5
Q

Plasma Relaxin Concentration in small animals

A

Values elevated in pregnancy from day 25 onwards and are diagnostic whilst a viable placenta is present

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6
Q

describe what can be felt on abdominal palpation in the bitch

A

From 21 days
Before this, the pregnant and non-pregnant uterus is not reliably palpated

Day 21 – 32
Aprox 1.5-3.5cm, round, firm and well separated
“Chain of walnuts”

After day 32
Gestational sacs become more confluent and lose their distinction - “sausages”

After day 50 the puppies may be balloted directly

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7
Q

radiography for small animal pregnancy diagnosis

A

Limited use in early pregnancy
Fetal calcification after day 41-44 (av – 42d)
So radiographic diagnosis from day 45
Can determine number, position and relative size of fetuses from day -50
Valuable in dystocia cases

Fetal skeleton – >day 42
Skull day 45-59
Pelvic bones day 53-57
Teeth day 58-63

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8
Q

ultrasonography for small animal pregnancy diagnosis

A

Fetal structures from day 17
Fetal heartbeats detected from approx. 24-28 days of pregnancy
Cannot assess number of fetuses

Has limitations, particularly in early gestation
Cannot be accurately used to count foetuses
Fetal heart movements 28-30 days after ovulation IF known
False negatives
False positives

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9
Q

what can be used to measure gestational age in small animals

A

Appearance of certain organs
E.g. kidneys last 20 days of gestation (see table for reference)

Measurement of foetal dimensions – less useful in later gestation
Gestational sac (or chorionic cavity) diameter in early pregnancy
Crown-rump length
Head diameter
Trunk diameter
Nb. These measurements are breed-specific

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10
Q

Pseudopregnancy

A

All entire non-pregnant bitches go through pseudopregnancy
Long luteal phase (~66d)
Clinical signs ->Prolactin
Covert/physiological
Overt/Clinical

Queen
Sterile matings
Behaviours less commonly seen
Hyperaemia of nipples as in pregnancy

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11
Q

Pyometra

A

Occurs during the luteal phase
Due to bacterial colonisation at oestrus
Can be open or closed
Most common in middle aged and elderly bitches
Pyometra may also be induced by:
therapeutic administration of oestrogens for treatment of unwanted pregnancy
therapeutic administration of progestogens for prevention of oestrus

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12
Q

Pregnancy Diagnosis (Queen)

A

Polyoestrous
Return to oestrous confirms non-pregnancy
BUT lack of return is not specific for pregnancy

Behavioural changes not useful
Physical changes.. Can be subtle
Reddening of mammary glands d21
Enlargement of mammary glands d50

Manual palpation – d21-25 optimal
Relaxin – d25
Ultrasonography – 3 weeks post mating
Radiography – mineralisation of fetal skeleton at d40.

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13
Q

treatment of Accidental Pregnancies

A

Surgical Approach

  1. Pharmacological Approach

Drugs that act on the uterus:

Oestrogens e.g. oestradiol benzoate
Alters transit time of zygote
Within first 5 days of mating

Anti-progestogens
Synthetic steroids that compete with progesterone
Aglepristone (Alizin)
Day 1 - 45

Drugs that act on the ovaries:

Prostaglandins – luteolytic
Bitch and Queen corpora lutea are ‘autonomous’ for first 15 days of luteal phase
PG’s of little use before day 20
Repeated treatments are necessary

Drugs that act on the pituitary gland:
Dopamine agonists (prolactin inhibitors) e.g. bromocriptine and cabergoline
No activity before 30d, moderate activity 30-40d

Suspected/Early pregnancy – Aglepristone
Mid-pregnancy 22-40 days – Aglepristone
Confirm by USS before and after (10d), repeat if necessary
Signs of parturition
Late pregnancy >40d after mating
PGF2a
Dopamine agonists
Combination

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14
Q

pregnancy diagnosis in the bitch

A

NOT a lack of return to oestrus
NOT elevated plasma progesterone
Trans-abdominal ultrasound: from day 25
Plasma relaxin: from day 25
Plasma acute phase proteins: from day 35
Abdominal palpation for discrete swellings: from day 28
Radiographic examination: from day 45

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15
Q

Predicting parturition in the bitch

A

A number of clinical indicators of impending parturition may be used, including:
Measurement of progesterone and LH during oestrous
Behavioural changes close to parturition-
Restless
Seek seclusion/excessively attentive
Inappetant
Nesting behaviour
Shivering

Clinical signs close to parturition- Relaxation of pelvic, perineal and abdominal musculature
Increased HR

Decline in body temperature
Measurement of progesterone in late pregnancy
Diagnostic imaging

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16
Q

Progesterone and whelping

A

Around ovulation assists in prediction of whelping dates:
the date on which progesterone first exceeds 1.8 ng/mL (~2 ng/mL) predicted the day of parturition within:
±1 day – 67% precision
±2 days – 90%
±3 days - 100%

Around due date:
<2.8ng/ml = 99% chance of whelping within 48 hours
<1.0ng/ml = 100%
>5ng/ml = <2% chance of spontaneous parturition within 12 hrs

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17
Q

stages of Normal Parturition

A
  1. Stage of preparation
    Production of relaxin (placenta)
    Causes relaxation of the pubic symphysis, vulval and perineal tissues
  2. First stage parturition
    Onset of contractions
    Restlessness, nesting, temperature drop

3.Second stage parturition
Expulsion of the foetus

4.Third stage parturition
Expulsion of the placenta and foetal membranes

  1. Puerperium
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18
Q

Maternal dystocia

A

Inadequate expulsive forces
Inadequacy of birth canal

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19
Q

Foetal dystocia

A

Presentation or disproportion (relative to the dam) of the fetus

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20
Q

dystocia- Defects of expulsive forces:

A

Intrinsic defects of uterine contractility
Nervous voluntary inhibition of labour
Failure of contraction due to mineral/hormonal imbalances (primary inertia)
Exhaustion of uterine muscle or depletion of pituitary oxytocin stores (secondary inertia)

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21
Q

dystocia- Defects in adequacy of birth canal:

A

Functional disturbances of genitalia e.g. incomplete cervical dilation
Obstructions e.g. neoplasia
Pelvic malconformations e.g. brachycephalics or past #’s

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22
Q

Management of primary inertia

A

Primary uterine inertia is the failure to initiate labor at term

Exercise to stimulate contractions
Digital stimulation (feathering) to stimulate endogenous oxytocin
Calcium borogluconate IV
No response to Ca -> oxytocin
Perform a vaginal exam
If not successful C-section

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23
Q

Management of secondary inertia

A

Secondary uterine inertia is the failure to progress once labor is initiated (uterine fatigue).

Correction of the cause of dystocia
Nothing
OR
Ca2+, oxytocin  C-sec as before.

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24
Q

Faulty foetal disposition

A

Presentation: longitudinal axis of the foetus and the maternal birth canal
Longitudinal (anterior/posterior), transverse (V/D)
Position: the surface of the maternal birth canal to which the fetal vertebral column is applied (D/V/LL/RL)
Posture: position of the appendages (flexion/extension of neck or limbs)

Disproportion:
Foetomaternal disproportion – when the foetus is larger than the capacity of the pelvis

Normal fetal disposition is described as cranial longitudinal presentation, dorsal position, extended posture.

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25
Q

When to get involved with dystocia

A

Second stage parturition
Expulsion of the foetus

Weak, irregular straining for more than 2– 4 hours
Strong, regular straining for more than 20– 30 minutes
Fetal fluid was passed more than 2– 3 hours previously, but nothing more has happened
Greenish discharge is seen but no puppy is born within 2– 4 hours
(red-brown in the queen)
More than 2– 4 hours have passed since the birth of the last puppy and more remain
The bitch has been in the second stage of parturition for more than 12 hours

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26
Q

Foetal distress

A

Normal fetal HR = 180-240 bpm
<180bmp = Foetal distress
Foetal HR <150bpm at full term = immediate intervention required

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27
Q

managment for dystocia

A

Establish a tentative treatment plan:
Conservative treatment
Manipulative treatment

Drug therapy-
Ecbolic (oxytocin)
Calcium
Tocolytic (clenbuterol-reduces contractions)

Surgical treatment-
Epidural anaesthesia
Episiotomy-enlarge birth canal
Caesarean operation

Euthanasia

Manipulative Treatment:
Repulsion-
Pushing the fetus out of the pelvis back into the abdomen to give more room (may be impossible if dam straining)

Correction-
Correction of the abnormal orientation

Rotation or version-
Alteration of alignment of long axis or transverse axis of fetus

LOTS of lubrication and a normal sized foetus required!

Traction:
Vectis forceps
Cup like structure over back of head of the fetus
USE WITH CAUTION

Medical management:
Ecbolic drugs e.g. Oxytocin
Contraindicated in cases of obstructive dystocia
Calcium gluconate

ONLY when:
Bitch is healthy
Cervix is dilated
Foetal size and positioning are appropriate
Foetal HR is normal

Emergency Cesarean Section indications:
Primary or secondary uterine inertia nonresponsive to medical therapy
Uterine rupture or torsion
Fetal malposition without success of correction by manipulation vaginally.
Fetal death with remaining viable but distressed fetuses.
Fetal distress with decreased heart rate.
150-180 bpm consider CS
<150 bpm – immediate CS

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28
Q

managment of Postpartum bitches/queens

A

Normal
Slightly elevated temperature (upto 39.2)
Serosanguinous vaginal discharge 3-6 weeks
Uterine involution 12-15 weeks

Abnormal
Temperature >39.5
Thick dark vaginal discharge
Haemorrhagic discharge more than a drop
Serosanguinous discharge >6 weeks

When to get involved-
Third stage parturition
Expulsion of the placenta

All the placentas have not been passed within 4– 6 hours (although placental numbers may be difficult to determine if the bitch eats them)
The rectal temperature is higher than 39.5°C (101.3°F)
There is continuing severe genital haemorrhage
The lochia are putrid or foul smelling
The general condition of the bitch is abnormal
The general condition of any of the puppies is abnormal.

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29
Q

comon female rabbit reproductive conditions

A

Normal pregnancy – need to know normal
Extrauterine pregnancy
Not uncommon
Escape of fertilised ovum or rupture of a pregnant uterus
Fetus becomes mummified
Dystocia
Rare

Pseudopregnancy
Reflex ovulators
Ovulation occurs approx. 10 hours after mating
Or by being mounted by another female  PSEUDOPREGNANCY
Lasts for 16-18 days
Territorial, nest building
Condition self-limiting

Pregnancy toxaemia-
Susceptible during late gestation
Predisposing factors = obesity, stress, reduced appetite
Depression, weakness, collapse, abortion, seizures and death
Diagnostics: history, clinical signs, acidic urine, ketonuria, proteinuria

Uterine disorders
Pyometra
Purulent vaginal discharge
Lethargy
Inappetent
Enlarged uterus palpable, ultrasonography, cytology, haematology, serum biochemistry

Mucometra
Build up of mucus within uterine lumen

Hydrometra
Build up of transudate fluid in the uterus
Weight gain, but decline in body condition, anorexia, respiratory compromise, abdominal enlargement
Clinical signs, ultrasonography

Neoplasia-
Uterine adenocarcinoma-
Most common tumour in female entire rabbits
Serosanguinous vaginal discharge or haematuria
Nonspecific signs -> anorexia, depression
Dyspnoea if pulmonary metastasis
Diagnosis -> palpation, radiography (chest as well), ultrasonography, histopathology
Often multicentric and involve both horns of the uterus
Metastasis via local spread into the peritoneum and other abdominal organs -> liver
Metastasis via haematogenous route  lungs, brain, skin or bones
Cystic mammary glands may be seen in association with this

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30
Q

pregnancy landmarks of rabbits

A

Gestation = 30-32 days
Often can gently palpate olive-sized masses from day 10
Fetuses can be seen on ultrasound from day 12
Fetuses difficult to feel abdominally from day 14
Parturition often day 30-32 – usually in the morning and quick
Fetuses will not survive after day 35

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31
Q

mamary gland disease in rabbits

A

Mammary masses
Progression from cystic mastitis
Development of irregular sized, fluctuant, subcutaneous nodules
Discharge – milk or amber fluid
Clinical signs, FNA and cytology
Mastitis
Lactating or pseudopregnant does
Common isolates
Staphylococcus aureus
Pasteurella spp.
Streptococcus spp.
Hot, swollen, firm, painful glands
Pyrexia
Depression
Clinical signs, culture and sensitivity.

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32
Q

male rabbit repro issues

A

Testicular tumour-
Seminomas, interstitial cell tumours, Sertoli cell tumours, lymphoma
Non-painful, firm, nodular testicular enlargement

Cryptorchidism-
Normally descend by 12 weeks
Scrotal sac does not develop on the side of the cryptorchid testicle

Orchitis and epididymitis
Bacteria  Pasteurella multocida
Viral  Myxomatosis

Trauma- Bite wounds, testicular evisceration and secondary infection

Swollen testes/scrotum, depression, anorexia

Venereal spirochetosis-
Treponema paraluis cuniculi
Redness, oedema, vesicles, ulcers, scabs around perineum and genitalia (+ face)
Clinical signs, microscopic visualisation, silver stains on biopsy, serological testing

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33
Q

repro disease in ferrets

A

Hyperoestrogenism (prolonged oestrus in entire female ferret)
Pseudopregnancy
Uterine disease
Pyometra, mucometra and hydrometra
Neoplasia
Mastitis
Prostatic disease
Adrenal disease (surgically neutered ferrets)

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34
Q

Oestrus cycle - ferrets

A

Seasonally polyoestrus.
Jills remain in oestrus until they are mated, or chemically brought out of oestrus, or the day length shortens.
Pro-oestrus indicated by increase in vulva swelling. Oestrus follows – will see large, swollen vulva & behavioural changes.
Prolonged oestrus = increases risk of persistent hyperoestrogenism development of pancytopenia due to bone marrow suppression.
Induced/reflex ovulators
Mating a rough process
Gestation 42 days
Litter size 6-8

Persistent oestrus ->pancytopenia
Subcutaneous and mucosal petechiae
Ecchymoses
Swollen vulva
Pale mucous membranes
Abdominal distension
Blood from cephalic vein
Poor prognosis

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35
Q

pseudo pregnancy in jills

A

Susceptible to pseudopregnancy ->implantation failure due to effects of photoperiod or lack of conception.
Associated with HCG injection or mated with a vasectomised hob
CS – weight gain, mammary enlargement & nesting behaviour.
Pseudopregnant jills may develop a fuller hair coat.
After the ‘whelping’ date  jill will cycle back to normal

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36
Q

adrenal disese in ferrrets

A

Correlation with surgical neutering
Increase in concentrations of gonadotrophins  loss of negative feedback  stimulation of adrenal cortex  adrenocortical hyperplasia and tumour formation
CS  symmetrical alopecia, ‘rat tail’, pruritis
Vulva swelling
Recurrence of sexual behaviour
Urinary incontinence  prostatic enlargement

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37
Q

repro considerations in gerbils

A

High incidence of ovarian disease
Ovarian cysts
Neoplasia
Clinical signs: abdominal distension, bilateral alopecia, weight loss, decrease appetite, respiratory effort.
Diagnosis: clinical signs, imaging

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38
Q

repro considerations in hamsers

A

Pyometra (hamsters & gerbils)
Care not to misinterpret in hamsters
Diagnosis: clinical signs, ultrasonography, cytology.

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39
Q

repro considerations in rats and mice

A

Neoplasia (mammary tumours)
Rats - subcutaneous fibroadenoma
Oestrogen and prolactin are thought to playa role in tumour development.
? Early neutering as a preventative measure

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40
Q

repro consideration in guinea pigs

A

Reproductive disease common
Cystic ovaries
Dystocia
Pregnancy toxaemia
Neoplasia
Cystic ovaries
Abdominal distension, lethargy, depression, bilateral alopecia in the area of the flank.
Cysts often contain clear fluid
May see subsequent uterine pathology
Diagnosis  Ultrasound

Dystocia
Fusion of the pubic symphysis in older sows that have not given birth  predisposes to dystocia
Normal parturition is quick (within 30 minutes)
Gestation 59-72 days (average = 65 days)
Clinical signs: unproductive contractions, straining, bloody-green/brown vulvar discharge

Pregnancy toxaemia
Last 2 weeks of gestation or the week following birth.
Acute onset lethargy, anorexia, dyspnoea, decreased urine production, acetone breath.
Hypoglycaemia, ketonemic, proteinuric and aciduric

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41
Q

How common is infertility in bulls?

A

Complete infertility
~ 5-10%
Sub fertility
20%+

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42
Q

Fully fertile mature bull running with 50 cycling healthy cows should..

A

60% in calf in 3 weeks

<10% empty after 9 weeks

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43
Q

Bull Breeding Soundness Evaluation

A

Physical exam- BCS, Heart &lungs, Eyes, Jaw, Lameness, Conformation, Abnormalities, External genitalia, Scrotal circumference

Semen analysis

Libido/service assessment

Infectious disease?

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44
Q

how is sperm assesed

A

Gross motility-
Grade 1-5
Beware dilution effect

Progressive motility-
% actively swimming forward
Beware temperature

New technology-
Dynescan

Slide preparation-
Eosin nigrosin stain
Smear
Microscope x 100

Wet prep-
Formal saline
Bioxcell

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45
Q

stages of labour in cattle

A

Stage one labour (start of contractions) : 8-12 hours
Stage two labour (from amniotic sac rupture to calf out): >2 hours
Stage three labour (passing of fetal membranes): 4-6 hours

Suggested intervention points during stage 2 (Oklahoma state research):
30 mins no progress cow
60 mins no progress heifer

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46
Q

Obstruction in cow partuition

A

‘Normal’-
Undilated cervix

Abnormal-
Undilated cervix
Uterine torsion
Pelvic abnormalities

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47
Q

Fresh cow check

A

Health check- Temp, smell, rumen fill, hydration
Appetite
+/- Ketones
+/- Vaginal exam

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48
Q

Metritis

A

Uterine infection post calving (~3 – 21dim, mainly 4-7d)
Voluminous purulent discharge
Smelly, red-brown usually

Involves the myometrium and the endometrium
Usually results in systemic illness-
Fever
Inappetence
Depression

Treatment:
Systemic antibiotics
NSAID
Fluid therapy
Energy – prop glycol

Herd situation?

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49
Q

Post Natal Check for cattle

A

Often around 30 days in milk

Two assessments:
Resumption of normal cyclicity
Uterus involuted and free of infection
Endometritis
Abscesses

Herd level assessment useful-
Proportion of cows cycling
Proportion of cows ‘dirty’

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50
Q

Endometritis

A

Uterine infection limited to the endometrium
>21dim
Often called ‘whites’ – white, purulent discharge
No systemic effects on cow health
~£160/case (AHDB)
Diagnosis – vaginal exam, metricheck, US
Treatment – if CL; PGF2a, or ‘washout’.

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51
Q

outcomes of a cow not seen bulling

A

90% - did

10%- Cystic ovaries-
Follicular cyst – thin walled, fluid filled structure >30mm diameter persisting on the ovary for >10 days in the absence of a CL
Luteal cyst/part luteinised cyst – wall thickness greater than 3mm

True anoestrus
Uterine disease- Chronic endometritis, pyometra, mucometra

Difficult to truly diagnose ovarian dysfunction at one visit!

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52
Q

Pregnancy Diagnosis in cattle - Techniques

A

Transrectal ultrasonography: >28 days
Manual palpation: >~35 days
Later gestation – fremitus, cotyledon bouncing
PAG testing – milk recording
Progesterone monitoring – eg De Laval VMS systems
Knocking
Non-return (animal does not appear to come back into heat)

Benefits of transrectal ultrasonography vs manual:
More accurate assessment of uterus (and ovarian structures)
Can detect twins
Can detect fetal heartbeat and assess viability
Less likely to cause iatrogenic abortion
Can sex embryos (55-60d)

Benefits of manual palpation
Cheap, no kit required
Possibly easier in later gestation than US

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53
Q

Conception Rate

A

Proportion of served animals Pregnant at PD
Not a true measure of fertilisation rate
(EED/LED)
AYR target >40%

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54
Q

Pregnancy Rate

A

Proportion of eligible animals pregnant in a given time period (usually 21 days)
PR = Submission Rate x Conception Rate
For example: (SR 60%) x (CR 40%) = PR 24%
AYR target: >20%

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55
Q

Fertility visit structure on a block calving farm

A

Clean checks
PSM -21d
PSM -7d
PSM +7d
PSM +21d
PDs
Different strategies

PSM= planned start of mating

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56
Q

Block Calving KPIs

A

Submission Rate: >90%
Conception Rate: >60%
3 week I/C rate: >50%
6 week I/C rate: >75%
12 week empty rate: <8%

Often AI and bulls

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57
Q

aims of calving with heifers

A

Aim to calve in well-grown heifers by 24 months
Which means they need to be I/C at 15 months
Heat detection
Synchronisation
Age at first calving KPIs…
Av vs %?
Better measures?
% 2nd lact?

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58
Q

Why would nutrients not be getting to the tissues?

A

Reduced Intake-

Not wanting to eat
Disease or chronic pain

Not able to eat
Dental disease or Dysphagia

Not being allowed to eat
Social hierarchy

Not being fed enough
Poor or Inadequate diet

Poor Absorption-

Inadequate presentation of nutrients
Dental Disease

Gastrointestinal Disease
Parasitism
Diarrhoea
Ulcerative GI disease
Inflammatory disease

 - Small Intestine, Colon, both Neoplasia
 - Lymphoma

Decreased Utilisation-
Disorder of nutrient metabolism
Liver Disease

Excessive Loss-
Protein losing enteropathy

Protein losing nephropathy

Increased Requirement-
Increased demand/Consumption
Bacterial infections
Chronic Viral infection
Neoplasia

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59
Q

Abdominal Ultrasonography In context of weight loss, can give information on;

A

Thickness of Small intestine and Colon
Assess characteristic of thickening
Are mural layers visible?

Peritoneal fluid volume

Presence of intra-abdominal masses

Liver evaluation (or u/s guided biopsy)

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60
Q

Gastroscopy In context of weight loss, can give information on;

A

Weight loss generally only present in more advanced cases of gastric ulceration
Altered or reduced appetite
Delayed gastric emptying

Other forms of GIT ulceration could cause weight loss through causing malabsorption
Right dorsal colitis associated with NSAID toxicity

Gastroscopic examination used to obtain trans-endoscopic duodenal mucosal biopsies
Indicated where there is evidence of small intestinal malabsorption

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61
Q

Abdominocentesis

A

Assess for presence of changes in peritoneal fluid

Low sensitivity, but good specificity for:

Peritoneal inflammation / Bacterial involvement
WBC > 5 x109/l
Protein concentration > 20g/l
Increased Lactate concentration
Serosanguineous colour change
Neoplasia
Rare to diagnose intra-abdominal neoplasia on PF alone
<50% solid tumours exfoliate cells
Usually presents as low grade peritoneal inflammation

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62
Q

Oral Glucose Absorption Test (OGAT) in horses

A

Simple and inexpensive test to assess absorptive capacity of small intestine

horse is fasted for 12 hours
baseline oxalate-fluoride blood sample are taken
1g/kg 20% warm glucose solution is given by stomach tube. bloods are taken every 4-5 hours or until return to base line
samples are analysed for glucose and the percentage abouve the baseline is calculated

Normal
Approximate doubling of baseline serum glucose 2 hours after dosing (70-100% increase)
Partial Malabsorption
15-65% increase in serum glucose at 2 hours, or slower to peak
Total Malabsorption
Serum glucose not increasing above 15% of baseline

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63
Q

Faecal Blood Test

A

Evidence of frank blood in faeces indicates colonic/rectal bleeding
(Upper GIT bleeding is digested in the colon so not represented in faeces)

Faecal Occult blood test
Detects albumin and haemoglobin separately
Proposed to differentiate between different sources of pathology
Varying evidence for diagnostic value

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64
Q

exotic Reproductive conditions – follicular stasis

A

Pre-ovulatory egg binding
Often seen in the older, female tortoise kept alone
If follicles are not resorbed -> inflammation of the follicles ->coelomitis
CS -> anorexia, HL paresis, generalised weakness

Due to an inability to produce progesterone  failure of regression of follicles.
Recent exposure to a male after a period of prior isolation?
Inappropriate diet?
Inappropriate husbandry?
Stress?
Lack of hibernation, light and temperature change?
Still in need of further research

Blood work – raised calcium, raised proteins
Ultrasonography
Advanced imaging

CT – follicles and shelled eggs- Follicle, helled egg

Ultrasonography - follicles

Treatment - medical-

Fluids
Nutritional support
Correct husbandry
Often surgical  hormonal implants ineffective for these cases

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65
Q

COELIOTOMY

A

Ligation – haemoclips or absorbable monofilament suture material
Closure - absorbable monofilament suture material
Skin closure
Everting suture pattern
Suture choice often non-absorbable and strong.
Skin suture removal not to be removed for at least 6-10 weeks

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66
Q

PLASTRONOTOMY

A

Heart : in the midline intersection of the pectoral and abdominal scutes.
Plastron hinge : often between the abdominal and femoral scutes.
Abdominal veins : parallel, running in a craniocaudal direction below the plastron

plastronotomy site between heart and plastron hinge

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67
Q

Ovariectomy in chelonians

A

The prefemoral approach- Preferred method if possible – less traumatic and faster recovery time
Useful in species with a larger prefemoral fossa
Craniocaudal incision is made in the skin
Blunt dissect underlying abdominal muscles
Dissect coelomic membrane
Closure – simple interrupted or continuous pattern for coelomic membrane, muscle and fat.
Closure – everting pattern for the skin

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68
Q

dystocia in reptiles

A

Non-obstructive factors
Lack of suitable nesting site
Stress
Hypocalcaemia
Infection of oviduct
Poor muscle tone

Obstructive factors
Oversized eggs
Malformed eggs
Oviductal stricture
Space occupying lesions

No presenting signs are pathognomonic for dystocia
No signs
Abnormal posture
Hind limb paresis
Anorexia
Malodorous cloacal discharge
Faecal or urinary retention
Cloacal organ prolapse

Treatment-
Fluids
Nutritional Support
Provision of nesting site
Calcium gluconate
Oxytocin-
Induces parturition/egg laying when uterine inertia is present (as long as there is no evidence of obstruction)
chelonians- Hydrate the tortoise  soak in warm shallow bath
Prepare suitable nest site
Calcium gluconate if appropriate
Oxytocin
SURGERY
Cloacal ovocentesis
lizards and snakes- More commonly seen in oviparous (egg-laying snakes) pythons, rat snakes, king snakes milk snake
Less commonly seen in ovoviviparous (live-bearing) snakes  boas, garter snakes

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69
Q

dystocia in birds

A

Dystocia
Caudal uterus
Vagina
Uterovaginal sphincter
EMERGENCY if compresses blood vessels and/or nerves
Radiography (conscious)

Treatment-
Stabilisation
Warmth
Fluid therapy
Calcium
PGE2 gel
GA -> manual delivery

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70
Q

Chronic egg laying in birds

A

Small psittacines -> cockatiels
Produce repeated clutches or a larger than normal clutch
Depletion of calcium and protein stores
Poor bone density
Weight loss
Pathological fractures
Dystocia

Environmental modification
Reduce photoperiod
Remove nesting material
Behavioural modification
Training
Leaving in eggs
Nutritional modification
Encourage foraging

Hormonal manipulation
Deslorelin (Suprelorin)
Desensitises GnRH receptors, thereby decreasing release of LH & FSH
Cabergoline (Galastop)
Potent selective inhibition of prolactin
May have beneficial effect in birds with chronic egg laying.
In birds it also conjectured that its action could be mediated via its effect as a dopamine agonist.
Leuprolide acetate (Lupron)
Leuprolide acetate is a synthetic nonapeptide that is a potent gonadotropin-releasing hormone receptor (GnRHR) agonist

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71
Q

breeding Soundness Exam for stallions

A

■ History
■ General physical evaluation-
Vision, cardiopulmonary, locomotor
Potential genetic/hereditary (e.g: parrot
mouth, cataract, chriptorchidism)
Blindness
lameness
Ataxia
Penis, prepuce
Penile paralisis
Scrotum and testes
Internal genitalia (manual palpation and
ultrasound)

■ Semen collection and evaluation ( 2
collections 1 h apart)
■ Libido and mating behavior
■ Examination of internal and external genitalia
■ culture of urethra/penile/fossa glandis
■ Ancillary procedures
■ Serology, virology, endocrinology, endoscopy,
genetics/karyotype

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72
Q

Estimation of Daily Sperm Output (DSO)

A

■ DSO is linearly related to
testis mass:
■ Mass can be estimated
by measuring testis
volume:
■ TV=0.52heightwidth
length
■ DSO=(0.024
TV)-0.76
(billions)

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73
Q

Semen Evaluation methods

A

■ Odour
■ Volume
■ Color
■ Sperm concentration (100-400 million/ml)
■ Total number of sperm
■ Sperm motility
■ Semen pH (optional)
■ Sperm morphology
■ Cytology - other cell types
■ Bacteriology / virology
■ Flow cytometry/fluorescence(advanced)

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74
Q

Sperm Motility

A

■ Subjective estimate:
■ Temperature
■ Dilution
■ Total motility
■ Progressive motility

■ Computerized motility analysis

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75
Q

Sperm Morphology

A

■ Classification systems:
■ Primary vs secondary
■ Major vs minor
■ compensable vs
noncompensable

■ Methods:
■ Stains (eosin-nigrosin)
■ FORMOL-saline wet
mount preparations
■ 1000x magnification

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76
Q

Oligospermia/azoospermia

A

■ Obstructive disease
■ Alkaline phosphatase
■ Testicular degeneration (Idiopatic or after
insult)
■ Testicular hypoplasia
■ Overuse

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77
Q

Diseases Of Scrotum, Testis And Epididymis in stallions

A

■ Hydrocoele/
haematocele
■ Inguinal hernia
■ Orchitis/epididymitis:
■ Trauma
■ Infectious

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78
Q

Thermal Injury To The Testis

A

Thermoregulation:
■ pampiniform plexus
■ cremaster muscle
■ scrotum
■ Spermatocytes appear most vulnerable to
thermal injury
■ Acute thermal injury may require 60 days
(duration of spermatogenesis) for recovery

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79
Q

Diseases Of The Accessory Glands

A

■ Vesicular adenitis (seminal vesiculitis):
■ Bulls
■ stallions
■ Prostatitis:
■ Dogs
■ Prostatic hyperplasia / neoplasia
■ Congenital defects (rare)

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80
Q

Lesions Of Penis And Prepuce

A

Trauma
■ common problem
■ paraphimosis
■ phimosis
■ rupture of corpus cavernosum
■ denervation

■ Congenital
■ Infectious

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81
Q

viral GI disease in cattle

A
  • Rotavirus
  • Coronavirus
  • Bovine Viral Diarrhoea
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82
Q

bacterial GI disease in cattle

A

E.coli
* Salmonella species
* Clostridia species
* Mycobacterium paratuberculosis (Johne’s)

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83
Q

Parasitic GI disease in cattle

A
  • Protozoal-
  • Cryptosporidium
  • Cocci
  • Worms-
  • Strongyles
  • Fluke
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84
Q

nutritional GI disease in cattle

A
  • Milk scours
  • Peri-weaning Scours
  • SARA
  • Grain overload
  • Dietary changes
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85
Q

Scour Check Kits

A
  • Used to detect common pathogens in
    young calves
  • Rotavirus, Coronavirus,
    Cryptosporidum & E. coli
  • Can be used on farm, results in 10
    minutes from small faecal sample
  • Easy to interpret - two lines positive,
    one line negative
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86
Q

Faecal Worm Egg Counts

A

Faecal Worm Egg Counts
* Preparation of faeces in a salt solution to
look for worm eggs or cocci oosysts
* Quick test to indirectly assess parasite
burden
* Test performed off farm either in-house
or sent off to external lab
* Used to look for gut worms and cocci
oocysts in youngstock & adults
* Can also be used in series to test wormer
efficacy

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87
Q

Faecal Culture for cattle

A

Microbiology for bacterial
causes of GI disease.
* Can be used for Salmonella,
Johnes, Clostridial toxin
detection and
Rota/Coronavirus
* Can be done in-house or sent
to external lab
* Can be slow to yield result

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88
Q

bulk Milk Surveillance

A
  • Used to monitor disease in
    adult cows
  • Can be used to monitor Fluke,
    BVD, IBR, Johnes, Salmonella
  • Useful comparing results year
    on year
  • Take into account vaccination
    status for some diseases when
    interpreting results
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89
Q

Windsucker Test

A

Part the vulvar lips and
listen for an in-rush of air
* Tests the integrity of the
vaginal vestibular sphincter in mares

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90
Q

Caslick’s ind

A

a x l

where a= the angle of declination of the mares external genitles compared to the anus
l= the effective leanth of the vulva

tests the nesesity of a caslick procedure

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91
Q

Caslick’s procedure

A

Vulvoplasty in mares

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92
Q

what can be felt on rectal palpation of the mare

A

Uterus:
– Size & symmetry (pregnancy,
pyometra)
– Tone (estrus, diestrus,
pregnancy)
– Contents (fluid, fetus)
– Other abnormalities (masses,
adhesions)

Ovaries
– Size & position
– Shape (ovulation fossa)
– Consistency
– Follicular activity
– CL not palpable
* Cervix:
– Length
– Tone (Estrus, Diestrus,
Pregnancy)
– Abnormalities (difficult to feel
rectally)

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93
Q

visual exam of the mare repro tract

A

peculum exam
■ Vaginoscopy
Allows to evaluate:
A. Changes in cervix during estrus
cycle

ESTRUS
■ Secretions ↑ (moist)
■ Vascularity ↑ (pink)
■ Relaxation ↑ (open)

B. Abnormalities
■ Anatomical
■ Accumulation material (urine, pus,
blood)
■ Inflammation (vaginitis, cervicitis)
■ Varicosities
■ Tears/Lacerations (cervix, vagina)
■ Adhesions

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94
Q

surgical Reproduction management of female mammles

A

‘Spay’ – removal of the ovaries and uterus.
Ovariectomy
Hysterectomy (total vs supracervical/subtotal)
Ovariohysterectomy
Ovariohystero-partial vaginectomy - rabbits

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95
Q

surgical Reproduction management of
male mammels

A

‘Castrate’ – removal of the testicles:
Scrotal-
Open
Closed

Prescrotal-
Open
Closed

Abdominal approach

Vasectomy
Vas deferens ligated and incised

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96
Q

medicla Reproduction management of mammels– male & female.

A

Medical management
Implants
Hormonal injections
Options vary depending on the species
Separation of the two sexes
Isolation of social species ->welfare implications
Housing animals of same sex may lead to fighting

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97
Q

reproductive managemnt of ferrets

A

Reproductive management of ferrets
Unique ->females must be taken out of season
If surgically neutered -> may predispose to adrenal disease

Pineal gland
A small conical endocrine gland
Attached by stalk to the dorsal wall of the third ventricle of the cerebrum
Major source of melatonin biosynthesis
Melatonin
Hormone synthesised and released during hours of darkness
Responsible for function of body related to photoperiod

Melatonin produced during dark phase of the day -> as longer days this suppression is lost-> get pulsatile release of GnRH Stimulates production of LH and FSH-> Stimulates the gonads to produce either oestradiol or testosterone.
Negative feedback on hypothalmus to prevent excessive secretion
What happens when we neuter them?
Loss of negative feedback-> Increase in the release of LH and FSH-> Persistently stimulate respective receptors in the adrenal cortex

Hobs usually reach puberty at approximately 9 months old
Jills reach sexual maturity in the first Spring after birth, at approximately 9 months old
Occasionally jills will show signs of oestrus in the first AUTUMN if
females were born early in the season
weather conditions are suitable
photoperiod is suitable.

Persistent oestrus  pancytopenia
Subcutaneous and mucosal petechiae
Ecchymoses
Swollen vulva
Pale mucous membranes
Abdominal distension

Natural mating (vasectomised male)-
Good option for owners/working ferreters with many jills.
Mating appears violent  biting and dragging the jill by neck
Pseudopregnancy lasts approximately 42 days
Increased aggression towards owners and cage mates
Abdominal enlargement
Mammary gland development
Risk of disease transmission if vasectomised hobs shared.
Will not change smell or hormonal behaviour
Leaves options for future breeding of the female

Delvosteron injection (jill jab)- Proligestone (Delvosteron, MSD Animal Health)
Suppresses/postpones the breeding season – maintains jill in anoestrus
Give 50mg per ferret in the Spring = 0.5ml per jill, administered via SC route
Signs of season often reduced within 10 -11 days
One injection often covers whole breeding season – but not always!
Pyometra risk
May be discontinued in 2023

Hormonal implant (Deslorelin)- (Deslorelin acetate)
GnRH agonist
Licensed in males (9.4mg), off license in females
4.7mg used in both sexes but off license
Reversible control of ovarian activity
Ovarian suppression for approximately 18-24 months
Easy to place as an outpatient
Brief GA
Placed SC between scapulae

Surgical neutering-
Ovariectomy or ovariohysterectomy depending on concurrent disease
Castration
Permanent method
Likelihood of developing adrenal disease.

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98
Q

reproductive managment of female rabbits

A

Spaying rabbits prevents
Unwanted pregnancies
Uterine disease
Cystic endometrial hyperplasia
Pseudopregnancy
Aneurysm
Neoplasia
Rabbits are sexually mature at 4-6 months
Neoplasia – adenocarcinoma  50-80% in certain breeds >4 years old
Free living European hares (feral) in Australia  21% of does had reproductive disease
Post mortem examination in pet rabbits
Mean year for neoplasia = 6 years
Youngest with neoplasia confirmed = 12 months.
Can we just perform ovariectomy?
Does depend on how early uterine disease can occur.
Anecdotally, reported in a 6 month old rabbit!

Unique anatomy
Two uterine horns
Two cervices
No uterine body
Long and flaccid vagina
Often large amount of uterine fat in mature rabbits
Vagina fills with urine during micturition

Techniques-
Ventral midline abdominal approach
Ovariovaginectomy often described
2 cervices, empty directly into the large vagina
Ligate ovarian pedicles and ligate at cranial vagina
Ligature placed around vaginal side of cervices
Risk of urine leakage through the vaginal stump
Must use a transfixing ligature
Oversew
Risk of including ureters and blood vessels supplying the bladder if ligature placed too low

Techniques
Ventral midline abdominal approach
Ligate ovarian pedicles and ligate around the uterine side of the cervices
Disadvantage
Leaves a small amount of residual uterine tissue
Advantages
Prevents the risk of urine leakage
Minimises the risk of infection from the vagina entering the abdomen  cervices are a natural barrier

Other points to consider
Prone to fat necrosis
Adhesions ‘internal scar tissue’ form around devitalised or traumatised tissue.
To minimise the risk of adhesions
Minimise tissue handling, always use instruments
Gentle surgical technique
Care with haemostasis
Never use dry swabs
Irrigate tissues with warmed sterile saline
Choose suture material wisely!
Use the finest suture material that is practical
Do not use biological sutures (cat gut)

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99
Q

reproductive managment of male rabbits

A

Medical reproductive management in rabbits is not used
Testicles descend into scrotal sacs at 10-12 weeks
Remember open inguinal ring
Options for castration
Scrotal
Open
Closed
Pre-scrotal
Open
Closed
Abdominal  Indicated for true cryptorchids

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100
Q

reproductive managment of female rodents

A

Reproductive management of rodents often requires surgery
Approach for the female
Traditional ventral midline
Flank
Flank approach – advantages
Less invasive
Quicker recovery time
Less risk of infection
Less risk of suture disruption and complications
Less risk of evisceration secondary to dehiscence of wound
Achieved via a bilateral or unilateral flank incision

Find your landmarks. Identify
The spine
The last rib
The pelvis
Gentle simultaneous pressure on these three points will produce a bulge of soft tissue in the centre  incision site.
Incise through skin (can be thick)
Blunt dissect through muscles
The external oblique
Internal laminar muscles

Once you have incised the muscle there will be internal fat
Fat will be associated with
The reproductive tract
The kidneys
The spleen
The GI tract

Retract the fat until you can see the distal uterine horn and ovary
Ligate the ovarian pedicle
In the guinea pig can perform whole procedure from the one incision
In the rat often a bilateral flank approach is required.

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101
Q

spaying in guinepigs

A

Ventral midline approach
Large incision needed
Challenging – deep body cavity, ovaries located cranially and dorsally
Longer surgery time
Longer recovery time
If large ovarian cysts can still perform flank approach
Remove fluid from cysts with a sterile needle and syringe.

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102
Q

reproductive managment of male rodents

A

Options for castration
Scrotal - true aseptic surgical preparation difficult
Open
Closed
Prescrotal - improved aseptic surgical preparation: requires 2 separate incisions
Open
Closed
Abdominal approach
Considered fertile for up to 8 weeks following castration

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103
Q

defences agianst mastitis

A

Defenses:
The Teat (Streak) Canal
Keratinocytes
Lipid secretions
Sphincter muscle
Phagocytes (somatic cells)
Frequent milking
Antibodies
Lactoferrin

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104
Q

clinical signs of mastitis in the individual cow

A

Abnormal milk and/or udder
Secretion
Size
Texture
Agalactia
Blind or non-functional glands
Hungry neonate
Pain – altered gait
Enlargement of the supramammary lymph nodes
Teat and skin lesions

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105
Q

California Milk Test

A

detects SUB-CLINICAL disease

thickening in the fluid indicates mastitis- degree of thickening is concurent with cell count

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106
Q

grades of mastitis

A

Classifications:
Peracute/ acute / chronic
Clinical / sub-clinical
Environmental / contagious

From a therapeutic perspective may be graded as
Mild - abnormal milk
Moderate - abnormal milk and abnormal gland
Severe - abnormal milk, abnormal gland, and sick cow

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107
Q

Septic mastitis

A

Most commonly caused by coliforms
Systemic signs of endotoxemia in severe cases
weakness, depression, inappetence
fever, scleral injection
tachycardia, tachypnea
rumen stasis, diarrhea
Endotoxaemia induces hypocalcaemia
Bacteraemia
Mortality common with endotoxic shock,
MODS

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108
Q

Summer mastitis

A

“Dry cow” or “Summer” mastitis, caused by Trueperella pyogenes
Most infections occur during the dry period
The incidence of infection is increased by filthy, wet, or muddy environments for dry cows
Purulent infection often leads to abscessation of the gland
The organism may be spread by flies

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109
Q

gi disorders in cows

A

Upper GI tract issues/Choke
“Hardware” disease
Acidosis
Ketosis
GI tract displacements/torsions-
Left displaced abomasum
Right displaced abomasum +/- volvulus
Caecal torsion
Small intestinal torsion

Enteritis

110
Q

Energy requirements dairy cow

A

Maintenance
Pregnancy
Milk production
Activity
Condition gain

111
Q

Fog fever

A

seen rarely in cattle grazing lush pasture. It is due to an excess of tryptophan in the diet which the animal can’t process quickly enough resulting in toxic damage to the lungs

112
Q

Farmers lung

A

an allergic reaction to the inhalation of fungal spores usually from mouldy silage

113
Q

club foot

A

in horses
conformation issue with hoof
Broken forward hoof pastern axis
change in digital cushion composure

risk factors-
Common digital extensor tendon injury
Navicular syndrome
Pedaloestitis

114
Q

Medio lateral imbalance of a horse

A

risk factors-
Collateral ligament injury
Articular cartilage damage
Degenerative joint disease
Sidebone
Corns
Sheared heels
Interference injury
Heel bruising/possible navicular syndrome

115
Q

Margination

A

Mesenteric fat highlights the serosal surface of the abdominal organs
Structures of the same opacity in contact with each other = border obliteration (border effacement/silhouette sign)

116
Q

Abdominal Contrast Studies

A

Contrast media:
Either more radiopaque or radiolucent than surrounding tissue
Document function by taking sequential still images (e.g. barium series) or using real time radiography (e.g. fluoroscopy)

117
Q

appearance of the liver on radiograph

A

Roughly triangular in shape with smooth distinct margins
Soft tissue opacity
Demarcated by the diaphragm cranially and the stomach caudally
Gastric axis should between parallel to the ribs and perpendicular to the spine (lateral) and perpendicular to the spine (VD)

Ventral lobe-
Fairly sharp angle- softer angle can idicate Hepatomegal
Extends to slightly beyond the level of the costal arch
May see gall bladder ventrally in cat

118
Q

Hepatomegaly on a radiograph

A

Projection of caudoventral margin well beyond the costal arch
Rounding of caudoventral angle
Caudal displacement of stomach axis

119
Q

meaning of a small liver on a radiograph

A

Cranial displacement of stomach
Absence of caudoventral angle
Significance dependent on clinical signs, etc.
Deep-chested dogs

120
Q

spleen apearence on radiograph

A

Location and size variable
Smaller in the cat (usually not visible on lateral views)
Flattened triangle on lateral view (tail of spleen)
Triangular mass next to left abdominal wall on VD (head of spleen)

121
Q

Splenomegaly on a radiograph

A

Generalised splenomegaly is common
Subjective assessment
Wide normal range
Overlap maximum physiological/ minimum pathological size
Spleen enlarges following ACP / barbiturates
Localised splenomegaly
Look for changes in shape as well as

122
Q

the stomach on radiograph

A

Rugal folds are often seen as parallel linear soft tissue opacities
If the stomach is completely collapsed and empty it may not be seen at all

Fundus and body lie to left of midline
Pylorus to the right and ventrally

Distribution of gas and fluid depends on the position

123
Q

small intestine on radiograph

A

Pylorus and duodenum are identifiable by location
Rest of small intestine fills “the space where there is nothing else!”

Cats tend to have less intestinal gas than dogs

Roughly even diameter throughout
Diameter in(dogs):
<1.4 x L5 unlikely obstructed
>2.4 x L5 likely obstructed

Look at the shape and distribution of the intestinal loops
Symmetrical peristaltic constrictions

Beware of “pseudo-thickening”
SI (or stomach) wall may appear thickened in plain images with partial filling with gas

124
Q

colon and rectum on radiograph

A

Often easy to identify because they are filled with faeces
However poor preparation limits interpretation

125
Q

Colic

A

Clinical syndrome associated with abdominal pain
Predominantly associated with GIT
May involve a number of body systems

Spontaneous recovery 28.7 %
Medical recovery 63.1 %
Surgical Recovery 2.0 %

Smooth muscle spasm
Inflammation-
Colitis / Ulceration

Distension-
Impaction
Gas accumulation

Obstruction-
Impaction

Tension on the mesentery-
Displacement

Tissue congestion/infarction/necrosis-
Torsion/volvulus
Strangulation

Inappetence
Reduced faecal output
Vocalising/grunting
Agitation
Pawing at the ground
Lip curling
Flank Watching
Lying down
For long periods
Repeatedly
Stretching to urinate
Rolling / Thrashing
Sweating excessively
Straining

Mild signs – Restless, Pawing, Flank watching
Gas build up / inflammation of GIT / Smooth muscle spasms
Moderate signs - Lying down flat out, groaning
Impaction or other simple obstruction
Very fractious, violent rolling
Acute, severe strangulation
Dull, unresponsive
End-stage – Severe illness due to colic

> 50% cases return non-specific diagnoses

Making a diagnosis is not as important as making an accurate assessment of the severity of the condition

Assess severity and duration
When was the horse last seen ‘normal’
Acute or chronic onset?
What signs are being displayed?
– persistent, intermittent, progressive?

Food and water intake since colic started
Faecal output
Has any treatment been administered?
Previous history of colic

Identify risk factors
Current management and any Recent Changes
Feeding
Stabling
Pasture access
Changes in exercise
Dental history
Parasite control programme
Vices

126
Q

‘Differential Diagnoses’ for colic

A

“False” colic
Any non-gastrointestinal source of abdominal pain
Liver disease / hepatomegaly
Urinary disease
Renal pain
Bladder Dz (urolithiasis)
Peritonitis
Intra-abdominal abscess
Intra-abdominal neoplasia
Reproductive disorders

Other
Non-abdominal, pain mistaken for colic
Oesophageal obstruction
Rhabdomyolosis (tying-up)
Laminitis
Pleuroneumonia

127
Q

factors that can be assesed or the prognosis of colic

A

Current status of colic-
Pain or signs of depression

Respiratory rate & depth
Abdominal distension
Presence of faeces

Evidence of duration / severity-
Traumatic injuries
Disrupted bedding
Shavings/soil on back

assessment of cardiovascular status-
a strong pulse, heart rate of 32-46, rapid jugular refil, pink mm and <2 sec capillary refil time is normal

higher heart rate, weaker pulse, slower jugular refil, darker mm and longer crt is indicative of edotoxemia from colic

Moisture content of oral MM is an assessment of hydration status;
Moist – Normal
Tacky or Dry - Dehydration

Compromised CV status is an important indicator for referral;
Deteriorating CV status is associated with poorer prognosis

Auscultation of GIT has some degree of specificity but low degree of sensitivity.
Hypermotility: Increased smooth muscle activity - ‘spasm’ colic
Local hypomotility: Localised stasis of GIT
General absence: GIT ileus – common finding in most colics
Very useful for monitoring cases – e.g. progressive loss of motility

Other assessment
Rectal Temperature
Most uncomplicated colics will have normal rectal temperature
Low core temp – usually associated with severe/end stage shock
Pyrexia – Can indicate alternate diagnosis, e.g. peritonitis

Digital pulses – not appropriate to assess circulation
– only useful to assess for presence of laminitis

Respiration-
Tachypnoea – usually due to pain, but could be associated with endotoxaemia (metabolic acidosis)
Detailed auscultation of lungs rarely necessary

Pain and colic assessment
Pain will only cause a mild-moderate increase in HR (40-60bpm)
Marked-severe tachycardia (>60bpm) is a sign of hypovolaemia
Pain will cause tachypnoea

Pain can make it very difficult to examine the horse
Administer quick-acting, potent analgesic
2-agonist
Xylazine (Rompun, Virbaxyl),
Detomidine (Domosedan),
Romifidine (Sedivet)
 opioid
Butorphanol (Torbugesic )
Try to assess CV status before giving 2-agonist

128
Q

Nasogastric Intubation

A

diagnostic for colic
Nasogastric reflux
Fluid/ingesta reflux from the stomach
>2 Litres of fluid is abnormal
Usually indicative of small intestinal obstruction (physical or functional)
Can occur due to LC displacement (pressure on duodenum)

Presence of gastric reflux has significant diagnostic value
Majority of cases with reflux need referring to hospital
Relieving reflux is also very therapeutic
>8L will stretch stomach and be a significant source of pain

129
Q

what is palpable on a trans resctal examination of a horse

A

ventral band of cecum
great vessels
caudal pole of left kidney
caudodorsal aspect of spleen
nephrosplenic space +/- ligamnet
fecal balls in small colom
uterus and ovaries
ingunal rings
bladder when full

Abnormalities: - Impaction
- Distension (Gas accumulation)
- Displacement
- Masses
structures palpable when abnomal-
deuodenum
jejunum
illeum
mesenteric root

130
Q

Abdominocentesis

A

diagnostic in colic

Assess for presence of changes in peritoneal fluid

Not indicated in every case

Serosal compromise – leakage of blood components- Serosanguineous colour change
Increased protein concentration

Anaerobic tissue metabolism -Increased Lactate concentration

Rupture of GIT tract- Presence of ingesta

Peritonitis

131
Q

analgesia for colic

A

Imperative to provide some form of analgesia to a colic case

NSAIDs
The most common form of analgesics used to treat colic
Slow onset and long duration of activity

Flunixin meglumine (Finadyne Solution)
1.1 mg/kg iv
Potent visceral analgesic
Can masks deterioration in CVS status

Ketaprofen (Ketofen)
1.1 - 2.2mg/kg iv

Phenylbutazone (Equipalazone Injection)
4.4mg/kg iv

Alpha-2 agonists-
Potent analgesics with rapid onset and short duration of action
Allow rapid re-assessment of case progression

Xylazine (Rompun, Virbaxyl)
Dose rate: 0.2-1.1mg/ml
Analgesia for 15-20min

Detomidine (Domosedan)
Dose rate: 0.01-0.02mg/kg
Analgesia for 1-2 hours

Romifidine (Sedivet)
Dose rate: 0.04-0.08mg/kg
Analgesia for 1-3 hours

Opiods-
Not first line analgesic
Usually reserved for higher degree of pain

Butorphanol (Torbugesic)
0.05-0.075mg/kg iv
Potent analgesic; 1 hour duration

Spasmolytics (Anticholinergics)-

N-Butylscopolamine (Buscopan Injectable )
Smooth muscle relaxant
Rapid onset and short duration of activity
Good for;
Treating hypermotile/spasm type colic
‘Gas’ colic
Relaxing rectum prior to rectal examination

General Rules
For first-line treatment, or where diagnosis is uncertain, use short acting analgesic agents
Assessing progression, rapid recurrence of pain or deteriorating CV status is vital in the decision to refer

Beware the potent anti-inflammatory effects of flunixin, which can significantly ‘mask’ the early signs of endotoxaemia.
Only administer NSAIDs after the diagnosis or CV status have been established

132
Q

when should colic cases be refered

A

Essentially, any indicators that the case won’t resolve with simple conservative therapy (analgesics & enteric fluids)

Non-response to analgesia
Significant CV compromise
Rapid deterioration despite therapy
Complex abnormalities on rectal exam
Presence of NG reflux
Recurrent/chronic cases with unclear Dx

133
Q

Periodontal disease

A

Periodontal disease is the most common disease in small animal medicine
> 87% of dogs and 70% of cats >3yrs.
May be obvious on clin exam  Radiographs to see true extent
See number of teeth involved and extent of involvement
Can then determine treatment options or use to monitor progression

134
Q

Dental disease

A

Clinical Signs of periodontal disease
gingivitis, plaque and calculus build up, gingival recession, bone loss, mobile teeth and eventually tooth loss.

Plaque: When bacteria collects within a matrix of salivary glycoproteins and extracellular polysaccharides and adheres to tooth surface
Calculus = tartar - when the plaque mineralises.

The bacteria and their by-products plus immune system = inflammation, infection and destruction of tissues

Plaque forms
Leads to gingivitis
Proliferation of plaque and deepening of the sulcus
biofilm accumulates  reduction in oxygen  transition from aerobic to anaerobic  toxins produced  immune response  tissue destruction and breaches junctional epithelium deepening the gingival sulcus
Further attachment loss
plaque mineralises, calculus forms  prevents healing and allows plaque to further colonise the tooth surface.
Tooth loss
the junctional epithelium separates, the tissues move away from the tooth surface, alveolar bones resorbs which causes the tooth to become mobile and eventually is lost.

135
Q

Mesial

A

toward the front midline of the maxilla or mandible

136
Q

Coronal

A

toward the tip of the crown of the tooth

137
Q

Periodontal probe

A

Blunt-ended, graduated instrument used to:
Measure attachment loss
Assess gingival inflammation through probing
Evaluate furcation lesions
Measure tooth mobility
Check for subgingival calculus/pathology

138
Q

Dental explorer

A

Sharp-ended instrument designed to give tactile sensitivity on hard tissue and is used to:
Detect softened enamel
Explore other defects, such as fracture sites and tooth resorption
Check the margins of restorations and crowns
Check for pulp exposure in GA patients

139
Q

Gingivitis index

A

Stage 0 – no gingivitis
Stage 1 – Mild – slight change in colour, no bleeding on probing
Stage 2 – Moderate – Redness and oedema, bleeding on probing
Stage 3 – Severe inflammation – ulceration, prone to spontaneous bleeding.

140
Q

Periodontal Grading Index

A

Stage 0 – Healthy periodontum, pink in colour, firmly attached.
Stage 1 – Gingivitis only due to calculus deposition, reversible by brushing/S+P, no attachment loss.
Stage 2 – upto 25% detachment loss, sulcus deepened
Stage 3 – 25-50% attachment loss,
Stage 4 – Over 50% attachment loss, disease has progressed, may see horizontal bone loss, severe inflammation

> 0.5mm in cats, >3mm in dogs = significant

141
Q

Furcation Index

A

“furcation” anatomical area where roots divide on multi-rooted teeth
Exposure = Indicator of severity of periodontitis

0 = no bone loss
1 = less than 1/3 bone of the width of the tooth lost
2 = more then 1/3 but not total
3 = open furcation

142
Q

Mobility Index

A

Loss of normal support around a tooth

0 – no mobility (<0.2mm)
1 = <1mm horizontal movement of the tooth
2 = >1mm horizontal movement of the tooth
3 = any vertical mobility

143
Q

Bisecting angle technique radiograph

A

Creating a shadow and capturing it
Identification of axes
Film “flat” or as perpendicular as it can be to tooth root
Measure angle between them
Cut the angle in half
Beam bisects this angle
Too steep = short/compressed image = miss pathology
Too shallow = elongated = exaggerate “normal”

144
Q

dental radiograph techniques

A
  1. Parallel technique
  2. Bisecting angle technique
  3. Extra-oral
145
Q

Parallel dental radiograph technique

A

Film parallel to target with a perpendicular beam
Simplest
Same as conventional radiography
Use for caudal mandibular teeth

146
Q
  1. Extra-oral dental radiograph techniquw
A

Cats
Caudally maxillary teeth
Superimposition of the zygomatic arch

Gives a skyline view of maxillary arcade

147
Q

Chevron sign

A

e widened periodontal ligament spaces in the apical areas of endodontically sound teeth, often in the shape of a chevron, resembling radiographic signs of apical periodontitis (Figure 14). This occurs most frequently at the maxillary incisors, canines, and mandibular first molar teeth.

148
Q

Vertical bone loss

A

Vertical bone loss was defined as the resorption of inter-dental marginal bone of at least 2 mm with typical angulation toward either the mesial or distal aspect of the root on intraoral radiographs.

149
Q

Horizontal bone loss

A

manifests as a somewhat even degree of bone resorption so that the height of the bone in relation to the teeth has been uniformly decreased, as indicated in the radiograph to the rig defects occur adjacent to a tooth and usually in the form of a triangular area of missing bone,

150
Q

Type 1 resorption

A

commonly begin resorption on the coronal third of the root, but can begin further apically. As resorption progresses, the coronal dentin often becomes involved. Eventually, dentinal loss undermines the enamel, causing it to fracture and resulting in a defect in the tooth.

151
Q

Type 2 resorption

A

radiographically the root appears to be disintegrating and not easily discernible from bone. This is referred to as replacement resorption.

152
Q

trauma in the tooth

A

Uncomplicated crown fractures = dentin exposure but not pulp

Complicated crown fractures = pulp exposure

153
Q

indications for toothe extraction

A

Periodontitis
Pulp Necrosis
Dental Fractures
Tooth Resorption
Cavities
Chronic Gingivostomatitis
Persistent Deciduous Teeth
Malocclusion
Supernumerary Teeth
Unerupted Teeth
Teeth Associated with pathologic lesions
Failed Endodontic Treatment

154
Q

Open extractions:

A

Require elevation of a mucoperiosteal flap and bone removal. Often with multi-rooted teeth, sectioning of the tooth into single-rooted sections.

155
Q

Closed Extractions:

A

Require neither but do require incision into gingival attachment and breakdown of periodontal ligament. Most commonly used in single root teeth.

156
Q

Diarrhoea:

A

altered pattern in normal pattern of defaecation
Increased:
faecal volume
water content
frequency of defaecation

157
Q

Osmotic Diarrhoea

A

results from the presence of osmotically active, poorly absorbed solutes in the bowel lumen that inhibit normal water and electrolyte absorption. Certain laxatives such as lactulose and citrate of magnesia or maldigestion of certain food substances such as milk are common causes of osmotic diarrhea.

158
Q

Secretory Diarrhoea

A

when electrolyte absorbtion is impared and the intestine does not complete absorption of electrolytes and water from luminal contents

159
Q

Increased gut mucosal permeability
leading to diarrhoea

A

guts let more than water and nutrients through — they “leak”

160
Q

abnormal gut motility leading to diarrhoea

A

abnormal muscle and nerve contractions that cause spasms or lack of motion anywhere along your gastrointestinal (GI) tract. Your esophagus, stomach, small and large intestine, as well as your colon and rectum may be unable to perform their functions in the digestive process leading to abnormal stools

161
Q

Acute Diarrhoea:

A

3 weeks
Change in diet
Diet history – raw feeding?
Scavenger? Table food?
Vaccination history (think age!)
Deworming history
In contact animals
humans with signs
How long its been going on for?
Character of D+ - etiology – SI, LI, mixed
Concurrent signs e.g. Weight loss, vomiting

Physical exam:
Dehydration?
Cardiovascular status?
Rectal temperature normal?

Oral exam
Abdominal palpation
Rectal exam

Minimum database:
PCV/TP -> dehydrated

162
Q

SI Diarrhoea

A

normal to large volume
watery
Melaena- black stools that occur as a result of gastrointestinal bleeding. This bleeding typically originates from the upper gastrointestinal (GI) tract
borborygmi- a rumbling or gurgling noise made by the movement of fluid and gas in the intestines.
weight loss +/- vomiting
inappetance
*SI can still be urgent

163
Q

LI Diarrhoea

A

Urgency/increased frequency
straining/tenesmus
haematochezia
small volume passed more often
mucus
fresh blood
“incontinence”

164
Q

parasitic causes of dihorea

A

Essential to rule out
Shedding not continuous
Protozoa e.g. Giardia spp. – 3-5 day stool sample
ELISA

Helminth GI
Toxocara
Trichuris
Uncinaria

Faecal flotation

OR..
Fenbendazole 5-day course

165
Q

Adsorbants

A

May reduce diarrhoea
Efficacy not proven
Kaolin
Pectin
Chalk
Bismuth subsalicylate
Magnesium aluminium silicate
Activated charcoal
Alter intestinal flora/bind flora
Coat or protect mucosa
Absorb toxins
Bind water and possibly antiscretory

166
Q

Faecal analysis

A

Systemically unwell
D+ is acute & haemorrhagic
D+ is very severe
Multiple animals in crowded environment
Owner or pet is immunocompromised

Faecal – parasites – SNAP Giardia/ELISA
Faecal – virology– SNAP Parvo

Faecal for microbiology?
Bacteria – Salmonella, Campylobacter, Clostridia
(Viruses)

Faecal for parasites – OR JUST TREAT?
Nematodes
Cestodes
Giardia – multiple samples?

167
Q

Chronic Diarrhoea

A

in a well patient-
Dietary sensitivity/Adverse food reaction
Immunological reaction
Diet trials
Elimination trial
novel protein – a good diet history!!
Hypoallergenic
hydrolysed protein
Dietary challenge to elicit recurrence

LI  fibre

Any change in diet should be progressive
Owner compliance is essential

in an unwell patient-

Blood work-
Biochemistry- Panhypoproteinaemia (low albumin and globulin)  PLE
Haematology- Mild non-regenerative anaemia
Urinalysis  check for protein
Basal cortisol
Vit B12
TLI
PLI

Trypsin-like immunoreactivity -
Exocrine Pancreatic Insufficiency

Clinical signs:
Steatorrhea
Dramatic polyphagia
Weight loss

Indicated if:
All of above fails
Hypoproteinaemic
Significant weight loss
Neoplasia suspected

Endoscopy
Upper GI only
Ex-lap

Further work up..
Immunosuppressive trials
Antibiotic trials
Faecal transplants..

in cats-
A bit trickier!
Chronic>acute
Tritrichomonas – PCR
Hyperthyroid – run a T4

Primary complaint might just be weight loss

168
Q

Vomiting

A

Active expulsion of gastric/duodenal contents
Protective function

A common clinical presentation

Do not assume vomiting = GI disease!
A disease of many body systems

Can range from inconsequential to life-threatening

169
Q

Stages of vomiting:

A

Prodromal phase:
Nausea- Hypersalivation, Loss of appetite, Lip licking
Excessive swallowing

Retching-
Retrograde duodenal contractions
Rhythmic inspiratory movements against a closed glottis
Dilation of the cardia and low oesophageal sphincter

Expulsion-
Reduced oesophageal and pharyngeal tone
Contraction of abdominal muscles to actively expulse gastric/duodenal contents

Programmed, overlapping and coordinated events help minimise risk of adverse events such as aspiration

170
Q

The vomiting reflex

A

Two separate centres:
CRTZ-
Humoral pathway
chemical stimuli
BBB is permeable in the area of the CRTZ

Vomiting centre in brainstem-
Several brain stem nuclei
Receives nerve impulses via 2 (neural) pathways:
Central
Peripheral
coordinates and integrates vomiting
Also Vestibular apparatus- input for motion sickness

Substance P-
neurotransmitter
binds to NK-1 receptors

NK-1 receptors-
location: cell membrane
vomiting centre
CRTZ

171
Q

What causes vomiting via the peripheral nervoud system?

A

Abdominal visceral receptors, Dz/irritation of: GIT, biliary system, peritoneum, urogenital system
->Vomiting Centre (medulla oblongata)

172
Q

What causes vomiting via the central nervous system?

A

Cerebral cortex, cerebral dz, pain, anxiety, fear,
->
Vomiting Centre (medulla oblongata)

173
Q

What causes vomiting via the Vestibular system?

A

Motion
Ear Disease
Vestibular Disease
->
Vestibular system
->
CRTZ
4th ventricle
->
Vomiting Centre (medulla oblongata)

174
Q

What causes vomiting via the primeraly CRTZ
4th ventricle?

A

Drugs, toxins, uraemia, keto-acids, infection
->
CRTZ
4th ventricle
->
Vomiting Centre (medulla oblongata)

175
Q

dietary causes of vomiting

A

change of diet
spoiled food
food intolerance
food allergy
immune mediated
types I, III and IV
proteins (glycoproteins)

176
Q

causes of vomiting in the stomach

A

inflammatory-
“gastritis” (acute or chronic)
ulceration

physical-
foreign body
outflow obstruction

functional-
motility disorder

neoplastic

177
Q

intestinal causes of vomiting

A

inflammatory-
inflammatory bowel disease

physical-
foreign body
intussusception
Volvulus

Functional-
Ileus

neoplastic

178
Q

abdominal causes of vomiting

A

pancreas (examples only!)- acute or chronic pancreatitis

peritonitis-
liver disease (examples only!)-
cholangiohepatitis
biliary obstruction +/- rupture

Renal disease-
AKI/CKD
Urinary tract obstruction

Uterine e.g. pyometra
Prostatic disease

179
Q

metabolic causes of vomiting

A

Hyperthyroidism (cats only)
Uraemia
Hypoadrenocorticism
Diabetic ketoacidosis

180
Q

central/cns causes of vomiting

A

Motion sickness
Vestibular disease
Encephalitis
tumours

181
Q

bacterial causes of vomiting

A

Salmonella
Clostridium perfringens
E.coli
Campylobacter jejuni

182
Q

viral causes of vomiting

A

Parvovirus
Feline panleukopenia
FELV/FIV/FIP
Distemper, Canine adenovirus

183
Q

parasitic causes of vomiting

A

Worms-
Toxocara
Taenia
Trichuris

184
Q

protoxoal causes of vomiting

A

Isospora
Cryptosporidium
Giardia
Tritrichomonas (cats)

185
Q

toxic and drug causes of vomiting

A

Antibiotics
NSAIDs
cyclosporine

Ethylene glycol
Raisins or grapes (dogs)
Theobromine
Ivy, daffodils, lilies
Conkers, acorns
Adder bites, toads

186
Q

Dysphagia

A

the medical term for swallowing difficulties
Clinical signs:
Gagging
Dropping food
Retching
Difficulty eating
Exaggerated swallowing
Ptyalism
Fear of eating

187
Q

Anti-emetics

A

Maropitant-
selective NK1 receptor antagonist
effective against
peripheral pathways
central pathways
Visceral analgesia in cats

Metoclopramide-
dopamine, 5-HT3 & H1 receptor antagonist
central>peripheral pathway effects
variable prokinetic effect
cats & dogs

188
Q

vomiting from a primary Gi problem should be uspected if…

A

An abnormality is palpable in the gut e.g. foreign body
The vomiting is associated with significant and concurrent diarrhoea
The patient is clinically and historically normal in all other respects
The onset of vomiting significantly preceded any development of signs of malaise – depression and/or anorexia.
The vomiting is consistently related in time to eating (although this can also occur with pancreatitis)

Primary GI disease diagnostics:
Survey and contrast radiographs
Abdominal ultrasonography
Endoscopy
Exploratory laparotomy

189
Q

vomiting from a secondary Gi problem should be uspected if…

A

Often have evidence from the history and/or clinical exam of abnormalities affecting other organ systems e.g. jaundice/PUPD
Vomiting is usually intermittent, unrelated to eating and may often occur subsequent to the onset of other signs of malaise.
Generally not usually bright, alert and happy.
Usually ill (depressed/inappetant) before vomiting was observed.

Exception to the rules: Pancreatitis.

Secondary GI disease diagnostics:
Biochemistry, haematology
Urinalysis
+/- imaging

190
Q

Megaoesophagus

A

recognize variations of normal (transient)
persistent abnormal dilation of the esophagus with gas or fluid
First line - plain lateral radiographs
+/- contrast radiography
+/- use fluoroscopy in cases of less severe or dynamic disease
Can be induced by anaesthesia/sedation/drugs

191
Q

Blood collection - chelonians

A

Jugular vein-
Less chance of lymphodilution
Often at level of auricular scale and base of neck
Apply pressure after

Subcarapacial sinus-
Haemodilution
Potential for damage to spine

Dorsal coccygeal vein-
Haemodilution
Potential for damage to coccygeal vertebrae

Brachial plexus-
Useful in larger chelonians
Extend front limb
Palpate tendon on caudal aspect of radial-humeral joint
Insert needle just caudal or ventral to the tendon

192
Q

Blood collection - lizards

A

Ventral tail vein-
Care with species that perform autotomy

Jugular vein-
Can be considered for leopard geckos

193
Q

Blood collection - snakes

A

Ventral tail vein-
Recommended site
Care not to insert needle into hemipenes or cloacal musk glands

Cardiocentesis-
CARE -> risks of laceration to ventricle and risk of pericardial haemorrhage

194
Q

Blood collection - birds

A

Venepuncture sites-
Right jugular vein
Can obtain large volumes
Gentle pressure to achieve haemostasis

Basilic (ulnar/brachial vein)-
Extend wing and visualise vein
Vein runs over the elbow area
Care as haematoma formation is common

Medial metatarsal vein-
Vein is very short in psittacines

195
Q

The 90% rule of cattle lamness

A

90% of the time it’s in the claw
90% of the time it’s on the back feet
90% of the time it’s the lateral claw on the back feet

hence easions most common on the hind lateral claws

196
Q

Foot trimming – Dutch 5 Step

A
  1. Toe length
  2. Match
  3. Model
  4. Create height
  5. Investigate/trim loose horn
197
Q

non infectious foot lesions

A

White Line Disease
Sole Ulcers

198
Q

infectious foot lesions

A

Digital derematitis
Foul in the foot

199
Q

White Line Disease

A

Degeneration of the horn at the white line leads to separation of the hoof wall from the underlying structures and weakening of the hoof wall

Risk factors:
Horn integrity
Surfaces
Stockmanship

Treatment:
Block other claw
Remove all loose horn
NSAID

Prevention-
Good cow surfaces
Good stockmanship
Appropriate nutrition

200
Q

Sole Ulcers

A

Disruption to horn growth due to pressure on the corium underneath P3

Risk Factors:
Standing time
Surfaces
Foot trimming
Fat mobilisation
Inflammation

log term isseus cause bone spurs

treatment-
Remove pressure
Block
Trim loose horn
NSAID

Prevention:
Cow comfort – minimise standing times
Maximise transition health
Ensure cows aren’t lame in dry yards
Prompt ID and treatment
Foot trimming technique and strategy

201
Q

Digital Dermatitis

A

Multifactorial
Strong bacterial component
Treponeme spp
Genetic susceptibility
Hoof hygiene!

treat active leasions (m2) topically and chronic inactive leasions with footbathing (m4)

202
Q

Foul in the foot

A

an acute and highly infectious disease of cattle characterised by swelling of the foot and resulting in lameness.

Treatment-
Systemic antimicrobials
NSAID
Local treatments

Prevention-
Similar to DD
Minimise risk of interdigital trauma

203
Q

claw horn disorders

A

white line leasion
soul ulcer
digital dermatitis
foul in the foot

Heel horn erosion- Prevention:
Hygiene and trimming of loose heel horn

Inderdigital hyperplasia
Toe lesions-
Thin soles!
Abrasion
Over-trimming

Fissures (hor,ver, axial)
Corkscrew claws-
Don’t tend to occur on well managed farms…

Medial corkscrew claws are a different phenomenon

Deep digital sepsis-Terminal presentation.

204
Q

Hoof health assessments

A

Not all feet need trimming!

Examine all cows 2x/year (more if required)-
Pre-dry off
Early lactation

Ensure foot trimming to a high standard

205
Q

Footbathing

A

3-4x/week
Not too strong/acidic (below pH3)
No more than 200 cows
Effective design required
Commonest ingredients – formalin, CuSO4

206
Q

Scald/Ovine Interdigital Dermatitis

A

Seen in sheep continuously exposed to wet pasture – often lambs but can be seen in housed ewes when straw becomes wet and warm
Fusebacterium Necrophorum – can be zoonotic – human wounds have been swabbed and F. Necrophorum found – wear gloves when examining lame sheep!
Mild and transient lameness, rapidly resolves with treatment
Dermatitis involving some or all of the skin between the claws of the feet – skin between claws appears red and inflamed with white discharge
V common, less important than footrot/CODD, but associated with pathogenesis of foot abscesses and foot rot

207
Q

Footrot

A

Footrot – 90% of lameness in the national flock
Dichelobacter Nodusus (Bacteroides) BUT needs F. necorphorum to facilitate epidermal invasion
D.nodosus – obligate parasite, can’t survive in the environment for more than 1 week
Also requires devitalised skin – chronic exposure to wet conditions and faecal contamination
Fly strike can occur in affected feet

early stage footrot – dermatitis and under-run horn visible

later stage, large amount under-run horn present

Very effective vaccine against footrot.
Acts as treatment and prevention.
Timing is important
A second injection can be needed 4-6 weeks
One injection will last 6 months.
Diagnosis is essential

identify risk periods and vaccinate before these (usually housing/lambing) or times of regular gathering.

Before high risk periods such as housing/lambing
This is where the vet comes in – doesn’t protetct against ay other form of lameness – if you are advising your clients to use it – be sure of the diagnosis!
H+S – make sure clients are aware of self injection risks – oil adjuvant in vaccine can cause unpleasant injection site reactions

208
Q

CODD

A

Contagious Ovine Digital Dermatitis
Relatively ‘new’ disease – ongoing research
Bacteria – treponeme species. Some association with cattle with Bovine Digital Dermatitis
Link between CODD and footrot
Usually SEVERE lameness with one claw of one foot affected
Initially ulcers develop on the coronary band which then under-run the hoof, can lead to whole hoof avulsion
Graded 1-5
Can lead to permanent hoof growth problems
Often needs systemic treatment with antibiotic and NSAIDs

209
Q

White line separation in sheep

A

Often individual rather than ‘whole flock’ issue
Unknown aetiology – walking on stony ground, nutritional imbalance?
‘Shelley Hoof’
Separation of the hoof wall from the underlying tissues
Lameness caused by dirt packing into space created
Can lead to abscess formation

210
Q

Toe Granuloma

A

Painful red swellings caused by:
Over-trimming
Chronic untreated lesions
Chemical irritation

211
Q

causes of lamness in sheep

A

foot rot
CODD
white line seperation
scauld/ ovine digital dermatitis
ORF
strawberry foot rot
bluetongue
Laminitis – all 4 feet, often after grain gorging or over-fat rams
Injuries – fractures etc
Neuro disease – spinal abscess
foot and mouth

212
Q

Joint Ill

A

Most common – Septic arthritis ‘Joint-ill;
Strep. Dysgalactiae, (e.coli, erisypelas sometimes isolated in older lambs)
Transmission still unknown – cord/tagging/tailing/castrating/oral/vaginal canal? Vaginal canal transmission thought to be most significant
Septic arthritis = swollen joints, ill thrift, death
1-2% of flocks, can be up to 50% of lambs in severe outbreaks
Lamb outdoors if possible! Reduces bacterial load for newborn lambs
Research evidence suggests that wearing long disposable gloves for lambing will be the most effective method to reduce the prevalence within a flock

213
Q

Gait assessment of horses

A

Hard straight line
Flexion tests
Soft and hard lunge
Ridden sometimes required

214
Q

Flexion tests?!

A

Thoughts?
Controversial amongst the equine population
Can induce lameness that may be unrelated to the baseline lameness
Responses must be interpreted carefully

How?
Apply stress or pressure on an anatomical region of the limb for set period of time
Horse then trotted off and observed for the effects of the test on gait

215
Q

What nerve blocks do we have available in the foot?

A

Palmar digital
Abaxial sesamoid
Coffin joint
Navicular bursa
DFTS?

216
Q

Palmar digital nerve block

A

What does it block?
Sole
Navicular apparatus
Soft tissues of the heel
Coffin joint
Distal portion of the DDFT
Distalsesamoideanligament

How?
25g 2/3in needle (25g if cobby!)
Needle separate from syringe
1.5ml mepivicaine
Proximal edge of the cartilage of the foot
Evaluate before 10mins

217
Q

Abaxial sesamoid nerve block

A

What does it block?
Foot
Middle phalanx
PIPJ
Distopalmar aspects of the proximal phalanx
Distal portion of the SDFT andDDFT
Distalsesamoideanligaments
Distal annular ligament
Fetlock

How?
25g 2/3in needle (25g if cobby!)
Needle separate from syringe
2.5ml mepivicaine
Base of the proximal sesamoids
Direct needle distally.

218
Q

Coffin joint block

A

What does it block?
Coffin joint!
Navicular apparatus
Branches of the palmar digital nerves
Toe region of the sole
(larger volumes – heel region of the sole)
Minimal benefit over PDNB

How?
20g 1.5in needle
Needle separate from syringe
5-6ml mepivicaine
Lateral approach with the limb off the ground
May be better tolerated
May enter navicular bursa or DFTS

219
Q

Navicular bursa block

A

What does it block?
Navicular bursa
Navicular bone and associated ligament’s
Solar toe pain
Distal DDFT
Does not block the coffin joint

How?
Hickman block
20g spinal needle
Desensitise skin
Ideally with radiographic guidance
Omnipaque?

220
Q

Digital flexor tendon sheath

A

What does it block?
Lesions within the DFTS
The portion of DDFT in the foot distal to the DFTS

How?
Palmar aspect of the pastern (out of choice)
Tourniquet applied
20g 1-1.5inc needle
Needle must remain superficial to the DDFT

221
Q

Nerve blocks limitations

A

False positive
Will the horse warm out of the lameness?
Proximal diffusion?
Clinician bias

False negative
Misdirection of needle outside of the fascia that surrounds the neurovascular bundle or into synovial structure.
Local anaesthetic inadvertently injected into a blood vessel
Clinician bias

Other limitations
Mechanical lameness that doesn’t respond to anaesthesia
Desensitisation of skin but not deeper structures.

222
Q

Foot balance radiographs

A

Gross imbalance can induce lameness
Correct early on in a lameness investigation
Leave the shoes on

223
Q

Lateromedial radiograph

A

How?
Foot positioned flat
Weight bearing on 2-5cm block
Horizontal beam centred on coronary band halfway between toe and heel
Dorso-palmar imbalance - Long toe/ low heel common finding

What to assess:
Solar surface angle in frontfeet
Long toe/low heel
Osteophyte/entheseophyteassociated with coffinjoint andnaviucularbone
Margin and cortico-medullary definitionnavicular bone

224
Q

Dorsopalmar (weightbearing) radiograph

A

How?
Leave shoes on
Foot positioned flat
Weight bearing on 2-5cm block
Horizontal beam centred on coronary band
Often foot not aligned with pastern/fetlock.

What to assess?
Medial –lateral imbalance – abnormal stress though the joints.
Coffin joint space should be even.
Ossification of the lateral cartilages

225
Q

Dorso proximal palmaro distal oblique radiograph

A

(Dorsal 65 degree proximal-palmarodistaloblique weight bearing–pedal/ navicular bone)

Shoes off–pack well with putty
Could useDPr-PaDiO
Standing on cassette tunnel
Some elongation of radiographic anatomy
Much easier to perform when limited people.

What to assess:
Navicular bone
Cyst like lesions
Distal border fragments and lucent zones
Medullary sclerosis
Pedal bone
Fractures
Keratomas
Osteitis

226
Q

Palmaroproximal – palmarodistal oblique of the navicular bone (skyline) radiograph

A

How?
Cassette tunnel
Caudal to the contralateral limb with heel on ground
45o angle
X-ray beam centred between the bulbs of the heel and collimated to the navicular bone

What to assess:
Palmar cortex of the navicular bone
Corticomedullary definition
Lucencies within the spongiosa
Cyst like lesions?

227
Q

MRI in equine medicine

A

Imaging method of choice in human medicine.
Every major hopsital is equipped with one
Used to diagnose everything from cancer to spinal and joint diseases.
In the equine veterinary world its being used to improve the accurary and efficacy of diagnostics for lameness investigations.

Radiographs show only bone
Ultrasound provides soft tissue detail
Ultrasound very limited in the foot.

Image bilateral limbs
Pre-fracture pathology and subtle soft tissue damage
Foot penetrations
Able to image within the hoof capsule!

Where radiographs are negative or unclear and US access is difficult in a localised area.
Penetrating injuries
When GA is unadvisable
Acute onset lameness during exercise
Cases that do not respond to treatment as expected.
Monitor progress/ readiness for competition.

228
Q

Computed Tomography

A

Series of x-rays emitted from various angles and the detectors measure attenuation
Provide a 3D image via advanced mathematical algorithms reconstructing the image

No super imposition or complex overlap of anatomy

Can orientate images to view key structures

3D image capture in 60 second scan time

229
Q

Gamma Scintigraphy

A

Radioactive technetium
Bone tracing agent
Identifying fractures
Poor performance cases
Difficult areas to examine/radiograph

230
Q

Sub-solar Abscess

A

The most common cause of acute lameness in horses
Ascending bacterial infection into the chorium (solar dermis)
Lesions in the white line
“Nail bind”
Penetration injuries
Risk Factors
Poor foot conformation
Seedy Toe
Wet, muddy conditions
Seen both in shod & unshod horses
Chronic Laminitis / PPID

Diagnosis
Acute & severe unilateral lameness
Grade 3 or 4 (AAEP lameness scale)
Increased digital pulsation to affected hoof – “Bounding pulses”
Heat in the hoof
+/- distal limb swelling

Repeatable and marked pain response on application of hoof testers

Differential Diagnosis
Solar Bruising, Pedal bone fracture,
Laminitis (rare to be unilateral)

TREATMENT

AIM TO ENCOURAGE DRAINAGE

Remove Shoe
Pare and clean the sole
‘Explore’ any discoloured tracts or defects in the white line
(Sedation infrequently required)​

NB: Nerve block contraindicated in NWB lameness

POULTICE
To soften hoof prior to curetting
To maintain drainage after abscess open
Poultice should be changed 2-3 times daily

Provide pain relief
24-48 hours NSAID therapy
Phenylbutazone 4.4 mg/kg IV or PO BID

Antibiotics are not indicated for un-complicated abscess

Tetanus Prophylaxis
Check tetanus vaccination status
If in doubt
->Administer tetanus antitoxin

Chronic Abscess-
Will rupture at coronary band or heel bulb
Still aim to encourage drainage distally
May require repeat flushing

Purulent Abscess-
Deeper/sensitive structure involved
Will require further diagnostics – Radiography
Likely to need more extensive surgery
Antimicrobial therapy indicated

231
Q

Solar Penetrations

A

If nail/wire is still in place
Leave it in situ - support leg with bandage/splint
Obtained radiographs if possible

If nail/wire already removed by owner
Try to identify tract and carefully pare sole to expose chorium (solar dermis)
Clean, lavage and dress the lesion
BEWARE delay in onset of lameness
Further investigations ASAP if any suspicion of complications;
Contrast Radiography/MRI

Potential Sequelae
Damage to Pedal bone
Pedal osteitis -> Sequestrum formation

Damage to Soft tissue structures-
Insertion of Deep digital flexor tendon
Impar Ligament

Synovial Infection-
Navicular bursa
Distal interphalangeal joint
Digital tendon sheath

Simple, uncomplicated penetration;
As per solar abscess – pare and poultice
Antibiotics only if clear evidence of infection
Judicious use of analgesia / NSAIDs
Penetrations with synovial penetration;
Broad-spectrum antimicrobial therapy
Procaine Penicillin, 22mg/kg IM BID (or IV QID)
Gentamicin, 6.6mg/kg IV SID
SURGICAL INTERVENTION
Arthroscopic lavage of synovial cavity

TETANUS PROPHYLAXIS

232
Q

Hoof Trauma

A

FOOT CAST-
Support
Sterility
Protection
Pain Relief

PRIORITIES-

Establish diagnosis to INFORM PROGNOSIS
Stabilise the limb
Provide analgesia

Situational awareness (finances, logistics, future athletic aims)
Allow owner to make informed decision on treatment
Prioritise welfare and recognize role of euthanasia

233
Q

Orthopaedic examination

A

Aims:
Localise bone/joint pain
Assess muscle atrophy
Localise crepitus
Assess joint ROM
Examine for joint effusion/thickening
Assess joint stability

Signs of pain:
Turning to look
Attempting to move away
Withdrawal of affected limb
Attempting to bite
Cessation of panting
Lip-licking
Fidgeting
Dilated pupils
Vocalisation

Palpation: Muscles, bones, joints
Symmetry (both legs at same time)
muscle atrophy
thickening
joint effusion
heat
pain

Manipulation:
May be painful – be gentle
Some manipulations better performed under sedation or general anaesthesia

instability: laxity (looseness), sub-luxation or luxation (dislocated)
pain
range of motion:
flex, extend, abduct, adduct, rotate
reduced or increased?
Crepitus

234
Q

lamness stemming from the distal limb

A

Both thoracic and pelvic limbs:
Paw pad!!
Corns in greyhounds
90% thoracic digital pads, digit III & IV

Be thorough
Examine individual digits, pads, interdigital webbing

Thickening of IP and MCP joints common in older dogs – may be incidental
Significance should be assessed by applying pressure and checking for pain response

235
Q

lamness stemming from the elbow

A

Complex hinge joint
Common site of lameness in large breed dogs:
Elbow dysplasia
Effusion  lateral epicondyle and olecranon

236
Q

lamness stemming from the shoulder

A

Biceps Tendon test
Abduction test to assess medial instability under GA/sedation

237
Q

lamness stemming from the pelvic limb

A

Tarsus-
Tibiotarsal joint only appreciable motion
Assess for laxity and luxations
Palpated and stressed
Hyperflexion
SDFT
Calcaneal tendon

Tibia & Fibula-
Deep palpation to elicit osseus source of pain
Detect focal area of swelling
Abnormal conformation

238
Q

Stifle Examination

A

Synovial effusion -> palpate either side of the patellar ligament.
Chronic cranial cruciate ligament instability results in medial fibrosis and thickening -> medial buttress
Patella position -> patellar luxation

239
Q

Stifle - CCL

A

Partial CCL rupture
Craniomedial band rupture
Cranial drawer only in flexion
Intact caudolateral band taut in extension – prevents cranial drawer

Caudolateral band rupture
No cranial drawer
Craniomedial band taut in flexion and extension – prevents cranial drawer.

240
Q

Stifle – Patella Luxation

A

Medial>Lateral patella luxation
More common in smaller dogs
Insidious in onset
Skipping intermittent lameness

Graded in severity from I to IV:
Grade 1: subclinical. Patella can be manipulated out of place but will return to its normal position
Grade 2: the patella luxates when the stifle is placed through a normal range of movement, spontaneously.
Grade 3: permanent luxation but the patella can be manually returned (reduced) to the femoral trochlear sulcus by the examiner, but the patella luxates again.
Grade 4: permanent luxation and the patella cannot be returned to the femoral trochlear sulcus.

241
Q

lamness in small animals origination from the hips

A

Hip examination:
Decreased ROM especially in extension
Crepitus
Pain
Laxity
Note -> Hip extension also results in extension of the lumbosacral joint and passive extension of the stifle – beware false-positives.
Extension and abduction of the hip = hip pain

242
Q

Ortolani test

A

More objective assessment of hip laxity
Must be done under sedation/GA

Angle of subluxation  the point at which the hip subluxates
Angle of reduction  the point at which the femoral head returns to the acetabulum

243
Q

Bone reacts to pathological processes in a limited number of ways

A

change in alignment
change in contour
increased or decreased bone mass.

244
Q

Abnormalities can be classified according to distribution within the skeleton:

A

Monostotic – involving a single bone (e.g. an osteosarcoma)
Polyostotic – multiple bones are involved (as seen with multiple myeloma or haematogenous osteomyelitis
Focal – may involve a specific bone region (e.g. the metaphysis)
Generalized – involving all bones (as may be seen with metabolic conditions)
Symmetrical or Asymmetrical

245
Q

Aggressive vs non-aggressive changes in bone

A

Aggressive lesion -> rapid bony change where there is minimal time for the bone to respond and remodel
Non-aggressive lesion -> benign, slow-growing, more chronic process with time for bone to remodel.
Wide spectrum in between!

This can be assessed by looking at the nature of any:
Bone destruction (lysis)
Periosteal reaction
Lytic edge character
Cortical disruption
Transition from normal to abnormal bone
Rate of change (10-14 days)

246
Q

Periosteal Reactions:

Aggressive vs non-aggressive changes

A

continiuos (solid, lamellar, lammalated)- least agressive
interupted (thick brush like, thin brush like, sunburst, amorphous bone production) - most agressive

New bone production:
Artifact (superimposition)
New bone production secondary to injury

247
Q

Bone loss or destruction- Aggressive vs non-aggressive changes

A

Patterns of bone lysis:
Artifact (superimposition)
Real due to generalised or focal bone loss

geographic lysis- least agressive
moth eaten lysis
permiative lysis- most agressive

248
Q

Stages of wound healing

A
  1. Haemorrhage/Coagulation -
    Immediate haemorrhage
    Vasoconstriction
    Vasodilation
    Blood clot forms
    ‘Scab’
  2. Inflammation/Debridement -
    6 hours after injury
    Neutrophils -> Monocytes -> Macrophages
    Macrophages – ESSENTIAL TO WOUND HEALING
    Wound exudate – serosanguinous to purulent – NORMAL finding
    Inflammatory phase can be minimal in apposed wound e.g. surgical incision
  3. Reparative .-
    Granulation tissue –
    Identified between day 3 and 5 of wound healing
    Fibroblasts
    Angiogenesis – capillaries advance 0.4-1mm/ day
    Collagen
    Develops from wound margins
    Contraction - 5-9 days after injury

Epithelialisation -
Visible 4-5 days after injury
Pink smooth margin to wound
Monolayer of cells

  1. Maturation
    Re-organisation of collagen
    Can take Months – Years
    80% Strength of normal tissue
249
Q

stage one of wound healing

A

Haemorrhage/Coagulation -

Immediate haemorrhage

Vasoconstriction

Vasodilation

Blood clot forms

‘Scab’

250
Q

stage two of wound healing

A

Inflammation/Debridement -
6 hours after injury
Neutrophils Monocytes Macrophages
Macrophages – ESSENTIAL TO WOUND HEALING
Wound exudate – serosanguinous to purulent – NORMAL finding
Inflammatory phase can be minimal in apposed wound e.g. surgical incision

251
Q

stage three of wound healing

A

Reparative-

Granulation tissue –
Identified between day 3 and 5 of wound healing
Fibroblasts
Angiogenesis – capillaries advance 0.4-1mm/ day
Collagen
Develops from wound margins

Contraction

5-9 days after injury

Epithelialisation

Visible 4-5 days after injury

Pink smooth margin to wound

Monolayer of cells

252
Q

stage four of wound healing

A

Maturation-

Re-organisation of collagen

Can take Months – Years

80% Strength of normal tissue

253
Q

First Intention wound healing

A

Healing of a wound where skin edges are closely re-approximated

254
Q

Second Intention wound healing

A

Gap left between wound edges and natural healing allowed to occur
nsuitable for surgical closure, extensive contamination or devitalisation

Allow to heal by granulation, contraction and epithelialisation

255
Q

Immediate Primary wound healing

A

Incision/Clean e.g. surgical incision
closes imediatly

256
Q

Delayed Primary wound closure

A

Clean contaminated – contaminated

closes Up to 2-3 days after wounding. Inflammatory phase over

257
Q

Secondary wound closure

A

Contaminated or Dirty

closes Up to 5-7 days after wounding. Granulation tissue present

258
Q

Approach to wound management in abrasions

A

= partial skin thickness wound

Rapidly re-epithelialise

Can be more severe – shearing injuries e.g. RTA

heals by Second Intention

259
Q

Approach to wound management in avulsions

A

Evaluation – Avulsion
= skin torn from underlying attachments e.g. de-gloving injury of distal

heals by
Delayed Primary Closure

Secondary Closure

Second Intention

260
Q

Approach to wound management in Incision

A

smooth wound edges with minimal trauma e.g. surgical wound
heals by Immediate Primary Closure

261
Q

Approach to wound management in laceration

A

= ragged incision with variable damage to surrounding tissues
Immediate Primary Closure?

Delayed Primary Closure

Secondary Closure

262
Q

Approach to wound management in burns

A

Classified by depth -

First degree: superficial

Second degree: partial thickness

Third degree: full thickness

Secondary Closure

Second Intention

263
Q

Approach to wound management in Punctures

A

e.g. bite wounds or ballistic missile

Minimal external skin damage
Extensive underlying tissue damage
Foreign material e.g. dirt/debris/hair in wound
Surgical exploration indicated
Consider underlying structures! - penetration of body cavities???

Delayed Primary Closure

Secondary Closure

264
Q

Poor local blood supply to a wound =

A

slow granulation tissue formation and increased risk of wound infection
Can be difficult to assess in the early stages

265
Q

Approach to wound management - debriding

A

Remove devitalised tissue, foreign material, bacteria from wound
Sedation/GA/local
Clip hair from around wound
SHARP excision with scalpel
Conservative with skin
Radical with fat/muscle
Preserve bone/tendons/blood vessels/nerves where possible
Bleeding good indicator of tissue viability
NO point leaving in obviously necrotic tissue

266
Q

Approach to wound management -Lavage

A

DILUTION IS THE SOLUTION TO POLLUTION

TYPE OF FLUID
TAP WATER – CHEAP and readily available. Useful for grossly contaminated large wounds

HARTMANNS/STERILE SALINE (0.9%) – fluid of choice. Still relatively cheap, minimally toxic to cells
20 or 50ml syringe with 18G needle

DO NOT USE UNDILUTED ANTISEPTICS E.G. CHLORHEXIDINE FOR WOUND LAVAGE

267
Q

Barriers to wound healing

A

Infection

Movement

Foreign Material

Necrotic tissue

Local factors – pH, Shape of wound
Poor blood supply

Health Status

Iatrogenic Factors

Cell transformation

Patient Temperament

Client Temperament

268
Q

Principles of Open Wound Management

A

Assess at every stage:
Degree of inflammation
Degree of exudate
Presence and quality of granulation tissue
Skin edges
Degree of epithelialisation

269
Q

Primary contact layer for Bandaging Inflammatory/Debridement
wounds

A

Wet to dry
Moisture retentive
Honey
Negative pressure
MagPrimary contact layer for Bandaging Inflammatory/Debridement
wounds gots
q24 hours for 1st 3 days then q48 hours

270
Q

Primary contact layer for Bandaging Reparative – early stages wounds

A

Wet to dry?
Moisture retentive
Honey
Negative pressure

271
Q

Primary contact layer for Bandaging Reparative – later stage/good granulation bed wounds

A

Moisture retentive
Foam/absorptive
Hydrogel if drying out

272
Q

Primary contact layer for Bandaging Maturation
wounds

A

Non-adherent
PU Foam
Change every 4-7 days