Horses Flashcards

1
Q

Within the special reproductive exam what is involved with the external exam

A

○ Note any discharge on vulva and tail (more common on the tail
○ Determine perineal structures: anus, perineal body and vulva should be in a vertical line
○ Vulva should be below ischeal arch
○ Parting of vulva lips should not lead to air being sucked into the vagina -> need to create a seal
○ Take clitoral swabs, if needed -> before rectal examination contaminates the area
○ Udder
§ Symmetry, activity (lactating or dry), fibrosis, acute inflammation, ticks

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2
Q

Endometrial biopsy when should be obtained and how

A
  • Should be obtained from all mares
    ○ That are valuable
    ○ That have been diagnosed with chronic endometritis
    ○ Where no specific cause of infertility can be found
    ○ That require expensive treatment: rectovaginal fistula repair, urethral extension
  • Induce biopsy punch manually into uterus, then move hand in rectum and push tissue into jaw of punch
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3
Q

what is important about interpretation of results from breeding exam

A
  • Only comment of BREEDING SOUNDESS NOT fertility
  • Breeding soundness certificate describes the mare’s chances to fall pregnant
  • Determine if tubular or endocrine disorder and if it can be treated
  • Discuss treatment plan and how success will be determined
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4
Q

What occurs with the equine source of progestagens

A
  1. The primary CL is the main progesterone horse in the equine pregnancy until about day 40 of gestation
    ○ Uterine progesterone
  2. The weight of the embryonic cups increases rapidly over the first 3 weeks
  3. The production of ecG (produced by the cups) is closely related to the weight of the endometrial cups
  4. ecG initially stimulates the primary CL to produce more progesterone
    ○ ecG is LH-like there results in luteinization of the follicles
    ○ FSH-like action in other species
  5. High circulatory ecG concentrations then lead to the luteinisation of more follicles resulting in accessory CL
    ○ At this point the pregnancy is considered more safe
  6. After day 100 the placenta takes over the role for the main production of progesterone (mainly other progestagens)
    ○ Now considered placental progesterone -> not actually high at this point
    ○ Equine placenta progestagens -> 5-alpa pregnanes -> main production from the placenta
    § THEREFORE total progestagens is measured not just progesterone as they will be low while total is high
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5
Q

Pregnancy loss and return to oestrus what is important at what days

A
  • Termination of pregnancy >34 to 37 days gestation (induced or natural) may not result in return to oestrus
  • Persistence of endometrial cups may delay return to regular cycles for 3 to 4 months (the cups continue to function and produce eCG; they survive until the time of their normal demise)
    ○ No foal heat and doesn’t come back into heat
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6
Q

Artificial/supplemental light why used, and how to achieve

A
  • Used to induce oestrus earlier in season
  • Required minimum of 60 days of stimulation (16 hours/per day) until well into transition (may need 90 days to result in ovulation)
  • Light has to sufficiently light whole area
  • Maintain under lights until diagnosed safely in foal
  • Same effects described with 1 hour of light applied exactly 9.5 hours after sunset
    Equilume
  • Mare out in the field with light shining into one eye, attached to the face mask
  • Need to ensure the light doesn’t move alignment or break -> labour intensive
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7
Q

Oestrus cycle average duration, standing heat, ovulation and dioestrus

A
  • Also have average oestrus cycle of 21 days
  • In standing heat for up to a week (4-8 days)
  • Ovulation occurs 1-2 BEFORE END of oestrus
  • Duration of dioestrus is usually 14-16 days
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8
Q

Suppression of oestrus when use and what use

A
  • Generally in the horse racing, competition environment
    1. Progestagen :eg. Oral regumate (once per day), longacting injectable
    2. GnRH vaccines’ follicular activity might not return -> should return after a few years as antibodies decrease
    ○ If never return -> problem!
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9
Q

Prostaglandin F2alpha what leads to and why wounldn’t this occur

A
  • Luteolysis achieved by single dose
  • Standing oestrus after 3 to 6 days
    UNLESS
    ○ Mare not in luteal phase (anoestrus, silent oestrus, transitional oestrus >35d pregnant)
    ○ In dioestrus, but less than 5 days ago
    ○ May take longer to come into heat if small/atretc follicles
    § Depends on where the horse is on its follicular waves, small follicles -> larger -> atresia (repeat)
    Granulosa (theca) cell tumor (GTCT)
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10
Q

Human Chorionic gonadotropin hCG how produced, function what occurs and when fails

A
  • Produced by the trophoblast cells of the human embryo placenta
  • LH-like function -> luteotropic -> keeps the corpus luteum around
  • Results in antibody production (probably don’t interfere with action)
  • If given at right time (35mm follicle, some oedema) 85% of mare ovulate between 36 and 42 hours
  • Might not work in transition when lack of LH receptors
    ○ Need sufficient oestrogen to produce LH receptors
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11
Q

GnRH analogues most common one, when use and what is important to remember

A
  • Most commonly used deslorelin (Ovuplant)
  • Ovulation between 42 to 48 hours if given as soon as largest follicle is 30mm
  • Implant should be removed to prevent downregulation of GnRH receptors (commonly placed in mucosa of labia)
    ○ If downregulated will take longer to get back into heat if conception is not successful
  • More expensive than hCG
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12
Q

What are some signs that a mare is ready to be bred

A
  • Ovulatory follicle: usually 30-32+/-mm of same size each cycle; can be large individual differences between mares
    ○ Generally don’t look for on commercial farms as just wait till she is ready to be induced
  • Increasing oedema
  • Cervix relaxes in oestrus, open until ovulation, then it closes
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13
Q

What is the AI dose

A

AI dose

  • 500 million progressively motile sperm
  • Sperm count (haemocytometre)
  • Motility assessment (heated phase contrast microscope) done at 37 degrees
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14
Q

Foal heat when present, when end, and what is the trade off

A

Foal heat
- Onset usually 6 to 9 days post foaling (5 to 12 days normal)
- Ends with first ovulation post-partum
- Interval becomes shorter later in season
- Higher early embryonic death rate if breed in foal heat (if OV before D10)
Trade-off between getting mare in foal as early as possible and ensuring successful outcome of pregnancy
- If breed in foal heat and successful actually gaining time (foal born earlier than last one)
- HOWEVER if breed foal heat but not successful then have to wait another 30 days to cycle again
○ Falling behind with schedule as if didn’t breed in foal heat would have short cycled her and then gotten pregnant earlier
WORSE if breed foal heat and successful but then LOSE pregnancy then you can be quite a lot of days behind

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15
Q

Success with frozen semen and ideal insemination time

A

30-35%/cycle
- Best management coupled with semen from a fertile stallion can yield results, equivalent to other methods (fresh, chilled): 75% + percent first service conception rate
- Mares that conceive with frozen semen mostly do so in cycle 1 or 2
○ If not by 3rd cycle, recommend switching to fresh or chilled (often successful)
Ideal insemination time: 12 hours prior to 6 hours after ovulation

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16
Q

What are the steps and the days which they are done for setting up AI with ovulation induction

A

Day 1: 8 pm (0 hours): deslorelin - induce ovulation (follicle between 30-35mm) - CAN’T HAVE LH SURGE
Day 2 (- 24 hours): scan mare to ensure she does not look like she will ovulate on her own
Day 3: 8am (36 hours): scan mare to ensure she has not ovulated - if she has just inseminate
Day 3: 2pm (42 hours): inseminate
Day 3: 8pm (48 hours): confirm ovulation
IF she has NOT ovulated
- Owner makes decision if that cycle is to be skipped or mare must be scanned every 6 hours to be inseminated again once ovulation is detected
- Mare should not be AI’d again until at least 18 hours after 1st AI (inflammatory uterine reaction)
○ shouldn’t inseminate until the next morning at 8am

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17
Q

Where is semen deposited, fertilisation occurs and transport of conceptus where

A
  • Sperm deposited into uterus
  • Fertilization in ampulla of oviduct
  • Transport of conceptus into uterus (5 to 6 days after OV)
  • Unfertilized ova remain in oviduct
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18
Q

When does fixation and implantation occur and what important about these

A
  • Fixation occurs at D 16/17
    ○ Stuck at the base of the horn
  • Implantation starts around D 35
    ○ When placentation starts -> attaches through endometrium
  • Nutrition through histiotroph (uterine milk) and yolk sac
  • Embryo is very vulnerable in this phase (EED)
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19
Q

What is the typical schedule for equine pregnancy scanning

A

Day 14 post ovulation (NOT INSEMINATION) - pregnancy & twin identification - HAS TO BE BEFORE DAY 16
Day 25 - 28 post ovulation - assess foetal viability (heart beat)
Day 40 post ovulation - confirm pregnancy (stud fee is usually due around this time)
Day 60 - 70 post ovulation - foetal sexing -> visualise the genital tubercle position
○ Only done by equine vets and need a 100% success rate as based on thousands of dollars
Day 150 - transabdominally sexing - external genitalia, penis, prepuce, teats, clitoris - not commonly done

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20
Q

Induction of parturition indicators, risk and what are the 2 main protocols

A
  • Very few indications -> Prepubic tendon rupture
  • Inform owner about risks -> risky for both mare and mainly foal
    Two protocols
    1. Normal protocol
    a. Give 10 IU of oxytocin IV
    b. If water doesn’t break within 40min: vaginal exam
    c. If straining for 10min without water breaking: incise chorioallantois
    d. If straining for 10min after water has broken: check for malpresentation/-position - in stage II labour
    2. Modified protocol
    a. Give 2.5 IU oxytocin IV
    b. If mare progresses to foal: RFB was in place
    c. If mare does NOT progress: postpone induction
    Helps prevent premature foals being born
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21
Q

Immunological castration how occurs, what used for and why not used much

A
  • Vaccine against GnRH equity
  • Only registered for use in mares NOT COLTS/STALLIONS
  • 10% of male horses -> became permanently infertile, doesn’t change behaviour of all male horses
    Should not use in animals intended for breeding in the fertility
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22
Q

What if there is male behaviour yet testes are not palpable or identified with US and castration history is unknown?

A
  1. > 18 months - anti-mullerian hormone produced by Sertoli cells
    ○ Simplest if at the right age
  2. < 2 yo or donkey of any age HCG stimulation test
    ○ Testosterone baseline and 30-120mins after giving HCG -> gelding <40 pg/ml, cryptorchid >100 pg/ml
  3. 3 yp Oestrone sulphate
    ○ Single blood test -> gelding <40 pg/ml, cryptorchid >400 pg/ml
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23
Q

What evaluating with sperm characteristics and stain used

A
  • Vol of the ejaculate (40-200 ml) x concentration = total sperm count. ( 500mill per dose)
  • Sperm cell morphology
  • pH of semen - 7.2-7.9
  • Bacterial cultures, e.g. for Taylorella equigenitalis(contagious equine metritis; CEM), Pseudomonas, Klebsiella spp.
  • Motility analysis (motility = % moving acitvely forward), chromosomal analysis, sperm chromatin assays, acrosome reactions etc.
    Stain nigrosineosin stained smear - black sperm DEAD
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24
Q

What are the 4 types of sarcoids and appearance

A
  1. Occult sarcoids, which are smooth, flat and usually hairless.
  2. Verrucous sarcoids, which have wart-like appearance.
  3. Fibroblastic or nodular sarcoids – these are sometimes referred to as two different types, with fibroblastic sarcoids usually being ulcerated and nodular sarcoids being lumps under otherwise normal-appearing skin. However, fibroblastic sarcoids are more likely a progression of the nodular form.
  4. Mixed sarcoids contain components of two or more of the above types. They most likely represent a transition between different types.
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25
Q

Melanoma treatment 3 options

A
  1. Surgery resection? -> anal sphincter issues
  2. Palliative care - intralesional chemotherapy
  3. Cimetidine - unsure on how works but can help
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26
Q

Rain scald (dermatophilosis) clinical signs, cause and how transmitted

A
  • Significant hair loss over face, dorsum, extending ventrally
  • Crusting bald/ulcerative
  • Housed outdoors, recent rainfall
  • No scratching/itching but painful
    Cause - Dermatophilus congolensis
    Required for development
    1. Moisture
    2. Skin abrasions
    3. A carrier animal
    Transmission
  • Flies, biting insects, fomites
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27
Q

Rain scald treatment and prevention

A
Treatment 
1. Wash with benzamidine, chlorhexidine 
2. Topical disinfectants 
3. Get horse out of the rain 
Prevention 
- Collect ulcerations as act as carrier of the spores 
Keep dry with adequate shelter
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28
Q

Dermatophytosis (ringworm) cause, transmission

A

cause - trichophyton and Microsporon - Warmth and humidity
Transmission
- Contact with other infected animals or infected hair shafts
- Younger animals more susceptible - immunity after exposure

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29
Q

Dermatophytosis (ringworm) treatment

A
  • Probably go away by itself but if want resolved quickly
    1. Malaseb - medicated wash
    2. Imaverol - systemic antifungal? - only if immunosuppressive - NOT IN PREGNANT ANIMALS
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30
Q

Pastern dermatitis predispoing factor and treatment

A

Predisposing factors
- Draft or feathered breeds
- Excess hair aids in keeping the area wet and prepetuation of bacterial growth
Also predisposed to chorioptic mange that can lead to dermatitis
Treatment
1. GET OUT OF THE MUD
2. Dry and clip the hooves
3. Topical disinfectants - dilute chlorhexidine scrub and topical ointments such as silversulfadiazine
4. Systemic antibiotics in severe cases -> procaine penicillin G
○ Should do culture and sensitivity if infection remains

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31
Q

Cutaneous habronemiosis what known as, cause and locations

A

Also known as “summer sores” due to increased occurrence during warm months
Cause
- Deposition of larvae Habronema microstoma/muscae or Draschia by flies (intermediate host) into wounds or moist skin sites rather than mouth (normally)
- Results in hypersensitivity reactions to dead and dying larvae
Locations
- Media canthus of the eye
- Third eyelids
- Distal limb
- Penis or prepuce

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32
Q

Cutaneous habronemiosis diagnosis, treatment and prevention

A

Diagnosis
Biopsy with histopathology usually revealing granulomatous inflammation
Treatment
- Ivermectin (moxidectin)
- Corticosteroids may be needed to control hypersensitivity reaction
Prevention
- Good fly control - with prompt removal and disposal of manure containing larvae and insect repellent application to affected and at-risk horses

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33
Q

Culicoides hypersensitivity “queensland itch” what results from, where located and age of onset in what climates

A
  • Hypersensitivity reaction to midge saliva proteins
    ○ May be a hereditary predisposition for developing hypersensitivity (most likely type 3 - antibody/antigen mediated)
    ○ Nature of the hypersensitivity response to unknown
  • Present mainly over the base of the mane, neck, dorsum and ventral midline
  • Age of onset usually 2-4 years and more common in warm, tropical climates - where midges are
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34
Q

Lice treatment what medications and how many applications

A
  • Most only kill lice and NOT EGGS -> 2-3 treatment administered 2 weeks apart
    ○ In order to kill emerging nymphs and adults from pre-existing eggs
    1. Ivermectin - administered systemically for SUCKING LICE ONLY
    2. Topical insecticides may be used FOR BOTH TYPES - fipronil and pyrethroids spray
  • Single application include imidacloprid (advantage)
    ○ Kill the larvae and adults
    ALL in-contact horses should also be treated
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35
Q

Atopic skin disease problem list

A
  • Severe pruritus -> due to antibodies cross-link mast cells, causing degranulation and release of inflammatory mediators
    ○ May not be present
  • Mild patchy alopecia
  • Seasonal
  • Secondary pyoderma may develop
  • Urticaria - “wheals” - transient focal swelling that result of dermal oedema arising from vasodilation
    ○ Found on the neck and cranial third of the body but may be diffuse over the body
    ○ Size variable from 1-10cm in diameter
    ○ Resolve if left untreated
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36
Q

Mites what are the 3 main ones, can they live off host, other animals infect and diagnosis

A

1) chorioptes bovis (leg mange) - can live off host, cattle, goats, skin scrape
2) psoroptes equi (body mange) - reportable disease, ear infestations, intense pruritis, skin scrape
3) sarcoptes scabiei (scabies or head mange) - rare, intense, burrow deep so may not on skin scapre may need biopsy

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37
Q

Mites treatment what are the 3 main steps and what NOT TO USE

A
  1. Shave their legs -> clip the feathers
  2. Ivermectin or moxidectin administered every 2 weeks for 2-3 treatments
    ○ Eggs will not be killed so need to do again (Same as lice)
    ○ Systemic Ivermectin and moxidectin may not eliminate all live mites - resistance possible
  3. Topical treatment - fibronil (frontline spray -administered once weekly for 1 month), lime sulphur, malathion
    - ALL in contact horses should be treated as well as DECONTAMINATION of fomites in the environment
    - NOTE -> Amitraz - DO NT USE IN HORSES
    ○ May cause ileus in horses that may be IRREVERSIBLE
    If in early stages -> alpha2 antagonists
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38
Q

Acute uveitis primary and secondary causes and treatment

A
  • Primary - equine recurrent uveitis
  • Secondary - to other ocular diseases
    Treatment
  • Treat primary cause
  • Timely anti-inflammatory therapy, corticosteroids, NSAIDS
  • Atropine
    Poor treatment = loss of vision
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39
Q

What are the 3 stages of wound healing and which are poor in distal limbs and therefore 3 reasons wounds break down in this area

A

Stages of wound healing;
1. Cellular debridement**
2. Proliferation/angiogenesis (granulation tissue)
3. Contraction/Epithelialisation
- ** poor in horse distal limbs
THEREFORE
1. Poor cellular debridement
/infection
- Horses > ponies
- Distal limb
2. Movement: Tension at suture lines
3. Orientation of skin vs blood supply - Upside down flap get tension in suture and will break down

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40
Q

Proud flesh treatment what are the 3 main ones

A
1) Trim with blade - no nerve supply 
○ Level with skin and distal 
○ WILL BLEED 
○ Removes superficial contamination/inflammation mediators 
○ Keep doing it time and time again until healthy and will close up 
2) Topical treatments 
○ Corticosteroids 
○ Yellow lotion - Zinc sulphate 
3) Movement prevention 
○ Bandages provide stability and promotes healthy granulation tissue 
○ Cast is optimal 
○ Bandage cast easier in the field
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41
Q

Chest wounds complications and treatment

A
Complications
- Subcutaneous emphysema* - SO COMMON WILL HAPPEN 
- Elbow joint sepsis
- Penetrate pleural space
○ Respiratory compromise
Treatment 
- Strict confinement
- Close/cover to reduce emphysema
- Daily lavage
- TAT, Abx
- Pneumothorax req emergency tx
42
Q

Carpus what also called, bones in proximal and distal row and the synovial structures

A

(knee)
Bones
Knee
- Proximal row -> (medial to lateral) -> radial, intermediate, ulnar and accessory
- Distal row -> first to forth carpal bones
○ The first is small and inconstant
Synovial structures
- Carpal sheath - surrounds both the superficial and deep digital flexor tendon as they pass the carpus
- Extensor tendon sheaths

43
Q

What are the 3 joints in the carpus and the pouches with how high motion

A
  1. Antebrachiocarpal joint (radiocarpal) -> high motion joint so will be able to feel
    ○ Palmar pouch - lateral aspect immediate palmar to the radius and proximal to accessory carpal bone
  2. Mid carpal joint -> high motion joint so will be able to feel
  3. Carpometacarpal joint -> low motion joint so won’t be able to feel (communicates with mid-carpal joint)
44
Q

Fetlock synovial structures and joint with pouches

A

Synovial structures
- Digital sheath - contains the deep digital and superficial digital flexor tendons as they pass the fetlock joint
○ Swelling will be palmar to the suspensory ligament and dorsal to the flexor tendons
Joints
- Metacarpo-phalangeal joint - has dorsal and palmar pouches
○ Palmar pouch -> between the third metacarpal bone and suspensory branch - most commonly see swelling here first
§ Common injuries -> suspensory branch tears, sesamoid fractures, palmar osteochondral disease
○ Dorsal pouch -> either side of the sagittal ridge of the third metacarpal bone -> swelling when more severe

45
Q

What is the main synovial structures in the hoof and pouches and the joint with its pouches

A
  • Navicular bursa - lies between the DDFT and the navicular bone
    ○ Proximal pouch - proximally on the dorsal aspect of the DDFT
    ○ Lateral and medial pouches - can be penetrated by deep wounds to the heel
    Joints
    1. Coffin joint (distal interphalangeal joint) - lies mostly within joint capsule
    ○ Dorsal pouch - extends above the coronary band axially 2cm
    ○ Palmar pouch - immediately dorsal to palmar pouch of navicular bursa
46
Q

What are the 5 nerve blocks of the carpus, what block and where inject

A

1) palmar digital nerve block - palmar digital nerve - collateral cartilage and palmar aspect pastern
2) Pastern ring block - palmar digital nerve and dorsal - midpastern under ergot
3) abaxial sesamod - palmar nerve - other sesamoid
4) low four point - palmar (b/n suspensory and deep) and palmar metacarpal nerve (under buttons of splint bone)
5) subcarpal nerve - lateral palmar metacarpal nerve (level of carpometacarpal joint

47
Q

Stifle what are the 3 joints, how interact and palpate

A
  1. Femoropatellar joint - swelling can be palpable between and overlying the patellar ligaments
  2. Medial femorotibial joint - palpated medial to the medial patellar ligament and cranial to medial collateral ligament
  3. Lateral femorotibial joint - deep so generally not possible to palpate swelling
48
Q

Tarsus (hock joint) what bones are present

A
  • Proximal row -> talus (has trochlea that articulate with cochlea of tibia) and calcaneus (sustentaculum tali -> DDFT)
  • Middle row -> central tarsal bone
  • Distal row -> tarsal bones 1-4 of which the first and second are fused, third rests on large metatarsal bone and forth is lateral and projects proximally into the level of the middle row
49
Q

Syonvial structure and ligaments and tendons within the tarsus

A

Synovial structures
- Tarsal sheath - through which the DDFT runs
○ Swelling is seen cranial, lateral and medial to the gastrocnemius and SFT tendons
- Calcaneal bursa - SDFT runs within
Ligaments and tendons
- Superficial and deep digital flexor tendons
- Plantar ligament - calcaneus to head of 2nd metatarsal bone
- Collateral ligaments - either side of tarsal joint

50
Q

What are the different nerve blocks with the tarsus compared to carpus

A
  • Similar to forelimb
    1. Palmar digital block - same
    2. Pastern ring block - same
    3. Abaxial sesamoid block - same
    4. Low 6-point block - slightly different
    5. Subtarsal block - similar
51
Q

What is involved with management of acute cases of laminitis

A
○ Treat cause
○ Pain relief - NSAIDS 
○ Minimise P3 movement
§ Restrict exercise - box confinement, deep bedding sand -> want them to lie down 
§ Sole support - Cast 
§ DDF tenotomy 
○ Cold therapy
§ Prevents mediators accessing laminae 
§ Only effective early - use prophylactically 
§ Involved lots of labour - 24 hour monitoring 
○ Sole support 
§ Dental impression material 
§ High density foam 
§ Wedge to reduce tension on DDFT
○ DDF tenotomy - incise 
§ The thing that is causing the pedal bone to rotate 
§ Salvage procedure 
§ May not improve long term survival
52
Q

Prognosis for laminits what does and doesn’t depend on

A
- Depends on:
○ Extent of tissue necrosis
○ Stabilisation of P3
- Not dependent on:
○ Degree of rotation
53
Q

Infammatory acute laminitis pathogensis and what is the general first presentation

A

grain overload
- How occurs -> ferment starch in caecum -> lactic acid produced will result in breakdown of the caecal wall allowing other toxins produced to get into the mucosa and access to blood stream -> changes in blood flow
○ Possible toxin includes matrix metalloproteinases -> produced in the hoof and responsible for breakdown of basement membrane resulting in causing sinking and rotation
First presentation - profuse watery diarrhoea

54
Q

Chronic laminitis ongoing management

A

1) Correct orientation of hoof capsule in relation to distal phalanx (P3)
- Allow well bonded lamellae to grow down from coronary band region
- Loss of use -> months - years maybe permanently - PREVENTION OF THIS
2) Restricted access to grass- Dirt yard; grazing muzzle
3) Antibiotics?
- Founderguard
4) Low GI diet
- No grain
5) Weight loss - control insulin and obesity in the equine metabolic syndrome
- Soak hay; 1.25 – 1.5% bwt (DM) /day
§ Careful not doing it too rapidly as can lead to hyperlipidaemia
- Exercise -> may be beneficial but diet the best

55
Q

ringbone what is it and the 3 locations present, which more common and associated with

A
  • Osteoarthritis with associated periosteal bone production on phalanges
  • Fibrous and then bony thickening
    1) Low-DIP joint
    § Not common
    § Often associated with intra-articular fractures or collateral ligament injury
    § Difficult to differentiate from other foot conditions due to poor specificity of IA (intra-articular) block
    2) High-PIP joint
    § More common
    § Chronic low grade lameness
    § Young horses –subchondral cystic lesions, fractures
    § Mature horses –chronic degenerative condition
    3) Non-articular - bony proliferation on pastern that isn’t associated with a joint
    Not common
56
Q

Superficial digital flexor tendon pathogensis of injury

A
  • Limited collagen turnover in adult tendon
    ○ Fatigue failure of collagen fibres occurs with repetitive loading
    § Higher strain leads to lower number of cycles to failure
  • Once injured -> Tendon repair
    ○ Type I collagen replaced with type II - NO TYPE 1
    ○ Well aligned fibres replaced with poorly aligned fibres
    ○ Increased tendon cross sectional area - typical scar - lifelong thickened tendon
    ○ Recurrence generally occurs at junction of normal and repaired tendon
    § Due to increased stiffness at injury leaving a difference in stiffness at junction
    -> stress concertation at this points
57
Q

Ultrasound evaluation of the lung what is it good at evaluating therefore diseases it can see and what is it not good at evaluating

A
  • Excellent for evaluating pleura and superficial lung
    ○ Pleural effusion
    ○ Superficial abscess
    ○ Consolidation
    ○ Pneumothorax - lack of glide sign
  • Does not penetrate aerated parenchyma
    ○ Unable to image deeper lung structures unless consolidated
58
Q

Trans-tracheal aspirate or wash what is it appropriate for, therefore what disease would you do for, additionally what part of the lung is sampled and what use sample for v

A
  • APPROPRIATE FOR CULTURE - most important way to do - WHEN THINK IT IS INFECTIOUS DISEASE
  • Pooled sample from entire lung
    ○ Good for focal lung disease - due to mucociliary clearance moving everything from distal lung up into trachea
    SAMPLE USED FOR
    1. Cytology
    ○ Variable neutrophils in normal horses (3 to 50%) - do get false negatives
    ○ May be bacteria present in normal TTW
    § Interpret in the light of evidence of inflammation
    § Intracellular more convincing of active infection
    ○ Fungal hyphae common in normal TTW
    2. Culture and sensitivity
    3. PCR can be useful for some pathogens
59
Q

Bronchoalveolar lavage where in the lung does it sample therefore which disease is it better for and not appropriate for

A
  • Samples a random, relatively small region of the lung
    ○ BETTER REFLECTS ALVEOLAR INFLAMMATION
    ○ Appropriate for global lung disease (RAO, IAD) - not focal disease
  • NOT appropriate for culture (pharyngeal contamination) - NOT FOR INFECTIOUS DISEASE
60
Q

EVH-1 and 4 when infected, how contagious, age of onset and why

A
  • EHV infection is ubiquitous in horses
    ○ Most horses infected in first year of life - respiratory
    ○ 80% seropositive
    ○ Highly contagious
  • Clinical disease common and occurs most frequently in weanlings, yearlings and young adults
    ○ Disease often seen after entry into a training stable
    ○ Mixing new animals, stress
61
Q

EVH-1 and 4 clinical signs associated

A
  • EHV-1 is also associated with Abortion storms (later gestation) and neurological disease
  • EHV-4 typically causes less severe respiratory disease - Upper respiratory tract disease - mucopurulent, bi-phasic fever
    ○ Very rarely causes abortion or neurological disease
62
Q

EHV-1 and 4 treatment and control

A

Treatment
- Symptomatic (anti-inflammatories to control fever)
- Rest from exercise essential
- Antibiotics
○ Typically not indicated
○ Prolonged (>7 days) or persistent severe clinical signs
Control
- Isolation of affected horses
- Immunity following natural infection not strong
- Vaccine immunity poor (required q3-6monthly booster)

63
Q

What are the 5 differentials for Bilateral nasal discharge, lymphadenopathy and fever and which want to rule out first

A
  1. Strangles - WANT TO RULE OUT FIRST AS VERY CONTAGIOUS
  2. Pneumonia
  3. Sinusitis
  4. Viral infection
  5. Pharyngeal/retropharyngeal/pulmonary abscess
64
Q

Streptococcus equi ssp equi (strangles) type of bacteria, age, how contagious and transmission

A
  • Gram (+) cocci - ALWAYS A PATHOGEN - should not be present
  • Mostly affects horses ages 1-3 years
    ○ However any age can be affected
  • VERY CONTAGIOUS
    ○ Spread by inhalation or ingestion
  • Fomites are very important in epidemiology
    ○ Buckets, water troughs, humans (veterinarians)
    ○ Does not persistent in the environment
  • Some horses will become persistent shedders
    ○ Reservoir in guttural pouches
    ○ Asymptomatic
65
Q

Strangles treatment for mild fever, anorexia and no respiratory distress -

A

○ Drain abscesses (hot packing - will rupture (once rupture very contagious particles released), lancing)
○ Cautious NSAID use -> in general with horses and gastric ulceration, possible dehydration for renal issues as well
○ Antibiotic therapy probably contra-indicated in mild cases and typically of little value once abscessation has occurred
§ Would use penicillin which is inactivated with puss

66
Q

Strangles treatment for severe respiratory distress with systemic signs of disease -

A

○ Often indicates retropharyngeal lymphadenopathy
§ +/- guttural pouch empyema
○ Antibiotics usually required
§ Penicillin is drug of choice
○ Tracheostomy might be required - if very extreme lymphadenopathy
○ Drain abscesses and treat guttural pouch empyema if present
§ Lavage, surgical drainage
○ Feeding tube, oesophagostomy etc might be required if severe, longstanding dysphagia present

67
Q

What are the 4 main complications of strangles

A

1) metastatic S. equi
2) bastard strangles - 10% abscess in brain, abdomen, liver, spleen - antibiotics 1-6months
3) pupura haemorrhagica - type III hypersensitivity reaction - vasculitis, distal limb oedema, skin sloughing - corticosteroids and penicillin
4) streptococcal myositis - rare, infarcts, immune-mediated

68
Q

Trephine what is it and when used

A

a hole to allow aspiration of fluid or biopsy - used for sinusitis (paranasl sinus empyema)

69
Q

Progressive ethmoid hematoma (PEA) what is it, how common, age, cause and clinical signs

A

mass (NOT A TUMOUR)
- Mass that grows via repeated hemorrhage - slowly expand
- Uncommon but important differential for epistaxis
- Typically middle aged to older
Cause - unknown
Clinical signs
- Low-volume, intermittent, unilateral epistaxis (rostral to nasal septum) or a serosanguineous nasal discharge unassociated with exercise.

70
Q

Progressive ethmoid hematoma (PEA) what needed for a definitive diagnosis, is this done and prognosis

A

Definitive diagnosis:
Histopathology
- But usually not biopsied as characteristic endoscopic appearance
Prognosis
- Good for a small lesion but poor for extensive lesions.
- Recurrence is not uncommon so warn owner that treatment is not curative in all cases and that annual or twice yearly endoscopic examinations are therefore recommended

71
Q

Progressive ethmoid hematoma (PEA) what are the 2 treatment options and which recommended and why

A

1) Chemical ablation via endoscope – inject lesion with 4% formalin on repeated occasions (every 2-4 weeks until the lesion is obliterated
- recommended due to reduced cost and avoidance of hemorrhage
2) Surgical resection of the lesion via a frontonasal bone flap approach -> uncommon due to risk of haemorrhage - laser better

72
Q

Gluttural pouch mycosis how common, why significant, cause and clinical signs

A
  • Can lead to death within 3 weeks
  • Very uncommon
    Cause - fungal growth within guttural pouch involved internal carotid artery (medial compartment) and/or external carotid and maxillary artery (lateral compartment)
    Clinical signs
    · Epistaxis - varies in severity from a minimal to litres of blood and is spontaneous
  • Other signs associated with damage to the various nerves - not as common
73
Q

Guttural pouch mycosis what important to consider before diagnosis and diagnosis

A

may be wise to consider referring the horse before endoscopic examination and prepare the surgery facility in case the clot over the artery is dislodged during the endoscopic examination
Diagnosis - endoscopy

74
Q

Guttural pouch mycosis treatment what is and isn’t effective and prognosis

A

Treatment
1. Surgical treatment is the only effective treatment and is an emergency as fatal bleeding can occur.
○ Refer promptly: 1st to fatal haemorrhage - 3 weeks or days
§ Involved occluding blood flow to the affected artery to cause regression
2. Medical treatment with antifungals is not effective if used alone
Prognosis with surgical treatment
- Good for survival (about 80%) but may be worse if nerve dysfunction is present (especially dysphagia) as this may not resolve.

75
Q

What nerve and muscle involved with the laryngeal hemiplegia

A

denervation atrophy of adductor and abductor muscles innervated by recurrent laryngeal nerve
- Cricoarytenoidous dorsalis muscle - ONLY ABDUCTOR muscle

76
Q

what are the 2 main displacements in the larynx

A

Dorsal displacement of the soft palate

epiglottic entrapment

77
Q

Inflammatory airway disease what age, how common and clinical signs (differentiate from RAO)

A
  • Young to middle-aged horses
  • Extremely common
  • Airway disease second only to musculoskeletal injury in wastage
  • 11-50% of THB and STB racehorses
    Clinical signs
  • Cough
  • Tracheal mucus
  • Exercise intolerance
  • Generally well and bright and happy - no increase in respiratory effort or rate (unlike RAO)
78
Q

Recurrent airway obstruction (RAO) what also called, main types where common, age and clinical signs

A
  • Also called Heaves
  • uncommon
  • Mostly indoor housing associated - moulds etc - not as common in australia as we don’t house inside
  • Summer pasture associated - possible pollens - more seen in australia
    § Feeding out from round bail hay - after been sitting there and have to move their muzzle all the way
  • Older horses
    Clinical signs - how to differentiate from inflammatory airway disease
  • Episodic (attacks) dyspnoea
  • Increased expiratory effort -> increase RR and HR
  • Cough
  • Heave line - abdominal muscle hypertrophy (increase) due to increased abdominal movement during expiration
  • +/- nasal discharge
79
Q

Equine asthma diagnosis and what not to diagnose with

A

Bronchoalveolar lavage - diagnose via percentage of neutrophils, eosinophils and mast cells
DON’T use skin testing or serum allergy testing as variable and not useful

80
Q

List the 3 main treatment options for equine asthma

A

1) environmental management - decrease dust/hay allergens
2) corticoeroids - RAO is progressive so needed here - systemic vs inhalaed
3) bronchodilators - not as sole treatment

81
Q

What are the 4 diagnosis technqiues for rhodoccous equi infections

A
  • Consider in any young horse showing signs of respiratory disease
    1. Clinical pathology indicating chronic inflammation
    ○ Hyperfibrogenaemia, leucocytosis
    ○ Increased platelet count
    2. Culture (and cytology) of appropriately collected tracheal wash samples
    3. Thoracic radiographs
    ○ Prominent alveolar pattern
    ○ Poorly defined regional consolidation and/or abscessation
    4. Ultrasonography
    a. Pulmonary abscesses in peripheral pulmonary parenchyma
    b. Very useful screening tool on endemic farms
82
Q

Rhodoccous equi treatment for mildly affected vs severely affected and treatment duration

A

MILD - Self-cure common
○ Screen weekly and ensure abscesses don’t get any bigger -> about 10cm below wouldn’t treat
SEVERE
- Macrolide antimicrobial
○ Erythromycin or clarithromycin
○ Adverse side effects - NOT IN ADULT HORSES
§ Colitis (often self-limiting), hyperthermia (erythromycin)
- Supportive care
○ Intranasal oxygen
○ Intravenous fluid therapy
○ Nutritional support
Treatment duration ranges from 4 to 10 weeks

83
Q

Pleuropneumonia/bacterial pneumonia what age, history of, clinical presentation and cause

A
  • Usually young adults
  • Often history of travel
    ○ Shipping fever
  • Clinical presentation
    ○ Dull, depressed, febrile, tachypnoea
    ○ Often no COUGH
    ○ Horses with pleurodynia can present with sign of colic
  • Causative bacteria are often opportunistic invaders from URT - why need to do trans-tracheal wash - strep equi ss zooepidemicus - MOST COMMON
84
Q

pleuropneumonia what are the 4 things needed for treatment

A

1) antibiotics - broadspectrum and change for culture results - pencillin and aminoglycoside +/ metronidazole (anaerobic - abscess present)
- need long-term treatment
2) NSAIDS - care with GIT renal
3) thoracic drains if necessary - until effusion stops
4) supportive care - IV, intra-nasal oxygen, nutritional, laminitis prophylaxis (ice boots)

85
Q

pleuropneumonia what are 4 complications and when do you stop treating

A

Complications
- Abscess formation (pleural, pulmonary)
- Pleural adhesions
- Jugular vein thrombosis
- Laminitis
When do you stop treating?
○ Re-check with radiographs and/or ultrasound
○ Normal fibrinogen and white cells count
○ Afebrile off all drugs for several days
- Mild cases usually require 1-3 weeks treatment
- Abscesses/necrotic lung/anaerobic infections will need 1-6 months
○ Need to switch onto oral antibiotics for this length of time will not handle intramuscular injection of penicillin for this timeframe

86
Q

Unilateral vs bilateral epistaxis where originate and examples

A

Unilateral - typically originates from URT
- Nasal passage
- Sinuses
- Guttural pouches (mild haemorrhage)
Bilateral - typically originates from LRT
- Exercise induced pulmonary haemorrhage
- Guttural pouches (moderate to severe haemorrhage)
- Larynx/pharynx
- Also consider systemic disease causing coagulopathies

87
Q

Exercise induced pulmonary haemorrhage diagnosis and possible treatment

A
  • Endoscopic examination of trachea within 90 min of exercise
  • Furosemide reduces the severity of EIPH
    ○ Reduces vascular pressures although exact mechanism of action is unclear
88
Q

in terms of aging foals up with 2 years old based on teeth what is involved

A

6 days: central incisors present
6 weeks: central and intermediate incisors present
6 months: all incisors present (corner incisors erupt)
12 months: dental star present in central incisors, corner incisors not in wear
18 months: corners in wear
24 months: dental star in all lower incisors, M2 present

89
Q

in terms of permanent dentition when central incisors, intermediates and corners erupt therefore when complete dentition

A

2.5 years: permanent central incisors erupted
3 years: centrals in wear
3.5 years: intermediates erupted
4 years: centrals and intermediates in wear
4.5 years: corners erupted
5 years: all incisors in wear (dentition complete at this age)

90
Q

Where do you find hooks and sharp edges

A

§ Hooks -> commonly develop on P2 upper arcade and M3 lower arcade
○ Maxillary aracade 30% broader and curved (compared to mandible)
- THEREFORE will get Outside (buccal) of maxillary (upper arcade) and inside (lingual) of mandibular (lower arcade) will get sharp edges

91
Q

what are the 2 main short-term visceral analgesics, their onset and duration, and when to use

A

○ Alpha 2 agonists: rapid onset, variable durations
§ xylazine: 20-30 minutes (200-250mg /500 kg IV)
§ detomidine: 40-60 minutes (0.5ml /500 kg IV)
○ Opiates: rapid onset, augments sedation
§ butorphanol: 30-40 minutes (0.5-1ml /500kg IV)
§ morphine: hours (avoided in colic: ileus)
- Use detomidine and butorphanol for severe pain
- Use xylazine alone for lower grade pain or procedures

92
Q

what type of drug used for longer term pain relief with colic, the 3 main drugs, duration and potency

A

NSAIDS
1) Flunixin: 0.5 -1.1mg/kg IV - most common
§ Duration 12-24 hours, onset 40 minutes
§ Potent visceral analgesic at high dose
§ Improves appearance of mmbs - keep in mind when reassessing horses
2) PBZ: 2.2- 4.4mg/kg IV
§ Duration 12-24 hours, onset approx 40mins
§ Less potent than flunixin for visceral pain - debatable
§ Oral phenylbutazone: 2 hours for effect
3) Buscopan: ‘Antispasmodic’ + weak NSAID -> not for significant GIT pain
§ Relatively poor analgesic compared with others

93
Q

What are 6 indications for surgery with colic

A

i. HR > 80bpm
ii. Cardiovascular compromise
iii. Zero gut sounds
iv. Not responding to flunixin (colic during 4-6 hours)
v. Abnormal rectal findings
vi. Serosanguinous peritoneal fluid

94
Q

Nasogastric intubation for colic what does reflex and lack of reflux mean

A

○ Any volume should be considered significant -> may be spontaneous or may need to create a syphon
§ SI obstruction**
§ Large intestinal distension; Impedes gastric outflow -> rare, only If large intestines are VERY distended
○ Lack of reflux? - what does it mean
§ Relative to duration
§ 16 hrs to back up

95
Q

Rectal tear during rectal exam what are the 2 main situations and treatment needed

A

□ Mucosa only
® Not normally a problem
® No further rectal exams
® Soften manure- enteral fluids
□ Mucosa + submucosa + muscular +/- serosa
® Needs definitive management
® Pen /gent/ flunixin/ propan B (decrease rectal movement) - OR give epidural
® Pack off rectum oral to tear - use damp cotton wool
◊ Damp cotton wool in stockinette 20cm oral to tear
® Broad spectrum antibiotics
® Get definitive treatment and communicate with the client

96
Q

Abdominocentesis location and what use

A

§ Most ventral part of abdomen
§ 2-3cm right of midline
§ Clip, prep, +/- local bleb/ stab incision (teat cannula) - ASEPTIC
§ 18G needle

97
Q

What are the 3 main treatments that need to occur in large colon impaction

A

1) Management
§ Pain relief: Flunixin or PBZ
□ Repeat doses not required unless severe
§ Soften ingesta
§ Promote motility
2) Enteral fluids: most effective - stomach tubes - parraffin oil + electrolyte drench - 6-8L / 500kg horse well tolerated
3) IV fluids in severe cases, systemic dehydration, or unable to tolerate enteral fluids

98
Q

Non-strangulating lesions what are the 2 main displacements

A

○ Right dorsal displacement:
- colon doges from right to left
§ Require surgery
§ And can progress to large colon volvulus
○ Left dorsal displacements
- nephrogenic entrapment of the colon (left kidney not seen in ultrasound)

99
Q

resection and anastomosis for small intestines what limited to

A

○ Limited to 50- 60% of total length (total 15-21m long)
○ Limited access to duodenum and distal ileum
○ Ability to resect depends on location
§ Resection can heavily influence prognosis

100
Q

Proggnosis for small intestines resections vs large intestinal

A

small - 60-70% survival

large - 50% survival - non-ischaemic 80%