Horses

Question 1

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

Answer 1

○ 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

Question 2

Endometrial biopsy when should be obtained and how

Answer 2

• 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

Question 3

what is important about interpretation of results from breeding exam

Answer 3

• 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

Question 4

What occurs with the equine source of progestagens

Answer 4

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

Question 5

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

Answer 5

• 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

Question 6

Artificial/supplemental light why used, and how to achieve

Answer 6

• 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

Question 7

Oestrus cycle average duration, standing heat, ovulation and dioestrus

Answer 7

• 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

Question 8

Suppression of oestrus when use and what use

Answer 8

• 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!

Question 9

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

Answer 9

• 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)

Question 10

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

Answer 10

• 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

Question 11

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

Answer 11

• 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

Question 12

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

Answer 12

• 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

Question 13

What is the AI dose

Answer 13

AI dose

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

Question 14

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

Answer 14

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

Question 15

Success with frozen semen and ideal insemination time

Answer 15

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

Question 16

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

Answer 16

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

Question 17

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

Answer 17

• 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

Question 18

When does fixation and implantation occur and what important about these

Answer 18

• 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)

Question 19

What is the typical schedule for equine pregnancy scanning

Answer 19

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

Question 20

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

Answer 20

• 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

Question 21

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

Answer 21

• 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

Question 22

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

Answer 22

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

Question 23

What evaluating with sperm characteristics and stain used

Answer 23

• 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

Question 24

What are the 4 types of sarcoids and appearance

Answer 24

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.

Question 25

Melanoma treatment 3 options

Answer 25

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

Question 26

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

Answer 26

- 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

Question 27

Rain scald treatment and prevention

Answer 27

``` 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 ```

Question 28

Dermatophytosis (ringworm) cause, transmission

Answer 28

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

Question 29

Dermatophytosis (ringworm) treatment

Answer 29

- 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

Question 30

Pastern dermatitis predispoing factor and treatment

Answer 30

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

Question 31

Cutaneous habronemiosis what known as, cause and locations

Answer 31

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

Question 32

Cutaneous habronemiosis diagnosis, treatment and prevention

Answer 32

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

Question 33

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

Answer 33

- 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

Question 34

Lice treatment what medications and how many applications

Answer 34

- 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

Question 35

Atopic skin disease problem list

Answer 35

- 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

Question 36

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

Answer 36

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

Question 37

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

Answer 37

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

Question 38

Acute uveitis primary and secondary causes and treatment

Answer 38

- 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

Question 39

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

Answer 39

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

Question 40

Proud flesh treatment what are the 3 main ones

Answer 40

``` 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 ```

Question 41

Chest wounds complications and treatment

Answer 41

``` 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 ```

Question 42

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

Answer 42

(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

Question 43

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

Answer 43

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)

Question 44

Fetlock synovial structures and joint with pouches

Answer 44

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

Question 45

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

Answer 45

- 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

Question 46

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

Answer 46

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

Question 47

Stifle what are the 3 joints, how interact and palpate

Answer 47

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

Question 48

Tarsus (hock joint) what bones are present

Answer 48

- 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

Question 49

Syonvial structure and ligaments and tendons within the tarsus

Answer 49

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

Question 50

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

Answer 50

- 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

Question 51

What is involved with management of acute cases of laminitis

Answer 51

``` ○ 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 ```

Question 52

Prognosis for laminits what does and doesn't depend on

Answer 52

``` - Depends on: ○ Extent of tissue necrosis ○ Stabilisation of P3 - Not dependent on: ○ Degree of rotation ```

Question 53

Infammatory acute laminitis pathogensis and what is the general first presentation

Answer 53

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

Question 54

Chronic laminitis ongoing management

Answer 54

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

Question 55

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

Answer 55

- 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

Question 56

Superficial digital flexor tendon pathogensis of injury

Answer 56

- 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

Question 57

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

Answer 57

- 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

Question 58

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

Answer 58

- 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

Question 59

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

Answer 59

- 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

Question 60

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

Answer 60

- 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

Question 61

EVH-1 and 4 clinical signs associated

Answer 61

- 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

Question 62

EHV-1 and 4 treatment and control

Answer 62

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)

Question 63

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

Answer 63

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

Question 64

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

Answer 64

- 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

Question 65

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

Answer 65

○ 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

Question 66

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

Answer 66

○ 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

Question 67

What are the 4 main complications of strangles

Answer 67

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

Question 68

Trephine what is it and when used

Answer 68

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

Question 69

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

Answer 69

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.

Question 70

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

Answer 70

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

Question 71

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

Answer 71

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

Question 72

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

Answer 72

- 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

Question 73

Guttural pouch mycosis what important to consider before diagnosis and diagnosis

Answer 73

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

Question 74

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

Answer 74

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.

Question 75

What nerve and muscle involved with the laryngeal hemiplegia

Answer 75

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

Question 76

what are the 2 main displacements in the larynx

Answer 76

Dorsal displacement of the soft palate | epiglottic entrapment

Question 77

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

Answer 77

- 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)

Question 78

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

Answer 78

- 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

Question 79

Equine asthma diagnosis and what not to diagnose with

Answer 79

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

Question 80

List the 3 main treatment options for equine asthma

Answer 80

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

Question 81

What are the 4 diagnosis technqiues for rhodoccous equi infections

Answer 81

- 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

Question 82

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

Answer 82

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

Question 83

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

Answer 83

- 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

Question 84

pleuropneumonia what are the 4 things needed for treatment

Answer 84

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)

Question 85

pleuropneumonia what are 4 complications and when do you stop treating

Answer 85

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

Question 86

Unilateral vs bilateral epistaxis where originate and examples

Answer 86

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

Question 87

Exercise induced pulmonary haemorrhage diagnosis and possible treatment

Answer 87

- 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

Question 88

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

Answer 88

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

Question 89

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

Answer 89

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)

Question 90

Where do you find hooks and sharp edges

Answer 90

§ 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

Question 91

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

Answer 91

○ 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

Question 92

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

Answer 92

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

Question 93

What are 6 indications for surgery with colic

Answer 93

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

Question 94

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

Answer 94

○ 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

Question 95

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

Answer 95

□ 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

Question 96

Abdominocentesis location and what use

Answer 96

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

Question 97

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

Answer 97

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

Question 98

Non-strangulating lesions what are the 2 main displacements

Answer 98

○ 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)

Question 99

resection and anastomosis for small intestines what limited to

Answer 99

○ 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

Question 100

Proggnosis for small intestines resections vs large intestinal

Answer 100

small - 60-70% survival | large - 50% survival - non-ischaemic 80%