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Horses Flashcards

1
Q

What things should be examined in a BSE of a mare?

A

Externally: udder, perineum, vulva, and clitoris
Internally:
-Rectal exam: carried out first, check uterus, ovaries, cervix, broad ligs and pelvis.
-Vaginal exam: manual and speculum, endometrial swabs for cytology and culture

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2
Q

When in the oestrus cycle should you take endometrial samples? Why? Are there risks?

A

In dioestrus (after d5). This is the time when the uterus is meant to be sterile and defence systems are at their lowest. (presence of bacteria/neutrophils in oestrus could lead to a false positive). By this time the oestral oedema should have also subsided making evaluation of biopsy sample easier. Need to follow up with PGF2alpha IM to eliminate risk of iatrogenic infection

Risks:uterus is susceptible to infection at this time

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3
Q

What are some indications for obtaining an endometrial biopsy?

A
  • valuable mare
  • mare diagnosed with chronic endometritis
  • when no specific cause of infertility can be found
  • expensive reproductive treatment required
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4
Q

What is a hysteroscopy?

A

Endoscopic examination of the uterine lumen. Helpful in dx of uterine cysts and adhesions

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5
Q

What is a starch granule test uses for?

A

To test oviductal patency

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6
Q

How long is the equine oestrus cycle? how long is doestrus?

A

21.5 d

14-16 d

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7
Q

What happens to hormone levels one a dominant follicle becomes a CL?

A

Declining inhibin and oestrogen, increasing progesterone, decline in LH

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8
Q

What are anovulatory haemorrhagic follicles?

A

Follicles which fill with blood but fail to ovulate. They eventually leutenize but may persist for several months and therefore prolong the interoestrus interval

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9
Q

What are some signs of oestrus in a mare?

A

Posturing (flexed hocks and stifles, arched tail, tipped pelvis)
Winking (everting clitoris rhythmically)
Urinating

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10
Q

How might oestrus be suppressed in mares to advance the onset of ovulation?

A
  1. Progestagens (eg. Regumate)
  2. GnRH vaccines
  3. Marble in uterus
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11
Q

What are different synchronisation techniques used in mares?

A
  1. PGF2alpha
  2. Progestagen
  3. Progesterone + oestradiol
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12
Q

How often should mares be teased?

A

Every day from 3 days post-partum until 60 d preg

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13
Q

What are some advantages of AI?

A
  • more mares can be bred to a single stallion
  • mare stallion don’t have to be in same place
  • limit disease transmission
  • breeding possible in otherwise incompatible unions
  • semen quality can be monitored
  • min contamination technique possible
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14
Q

What are conditions for motility assessment of sperm?

A

500 million progressively motile

Assess with contrast microscope at 37 degrees

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15
Q

How many days post foaling is a mare likely to show foal heat?

A

6-9 days post foaling

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16
Q

What must occur following pregnancy for a mare to be able to fall pregnant again?

A
  1. Uterine involution
  2. Shedding of bacteria
  3. Resuming regular cyclic ovarian activity
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17
Q

Should a mare be bred on foal heat?

A

Yes it she had a normal parturition/ puerperium and if she has ovulated on or after day 10 post partum.

No if opposite occurrences to this.

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18
Q

What are some principles of the minimal contamination technique with regards to AI?

A
  • Semen diluted with extender
  • Semen extended to a conc. of 25-50 million/ml
  • Mare should only be bred once per cycle and as long as possible before ovulation
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19
Q

What is the ideal time to inseminate a mare with frozen semen?

A

12 hours prior to 6 hours after ovulation (too much before that, sperm wont be good, too much after, egg quality declines)

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20
Q

If an AI attempt is unsuccessful, how long should you wait before trying to inseminate a mare again? Why?

A

At least 18 hours due to the risk of an infl. uterine reaction

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21
Q

What are some true indications for exogenous P4 therapy in a mare?

A
  • Endotoxaemia
  • High plasma cortisol levels
  • Failure of conceptus to signal MRP

(i.e anything that might cause luteolysis)

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22
Q

Where does fertilization in the mare occur? How long after ovulation?

A

In the ampulla of the oviduct

10-12 hrs

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23
Q

What is and what is the role of the capsule of an embryo?

A

Acellular membrane between trophoblast and zona pellucida. It is retained until the third week of pregnancy.

Protects the embryo during passage through the uterotubal junction and likely has a role in uterine-embryo interactions

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24
Q

When does fixation of the embryo occur and what causes it?

A

Day 16-17

Embryo size and uterine contractions

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25
Q

What is eCG?

When is it detectable in the blood?

A

Equine chorionic gonadotrophin- a protein hormone produced by the endometrial cups between d40 and 120. It has luteotrophic properties and leads to formation of secondary CL

Day 40-100

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26
Q

The embryonic bulge in a mare can first be detected via palpation at what day and where? What also happens at around this time?

A

D20 at the utero-cornual junction

Paling of vagina and cervix

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27
Q

At D21 on ultrasound, a small echogenic spot appears in the ventral part of the vesicle. What is this?

A

The embryo

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28
Q

When can the heart beat of the embryo be detected by US?

A

d23-24

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29
Q

Manual embryo reduction is best done by what day? What drugs may help with this procedure?

A

Prior to day 16 (mobility phase)

Propantheline bromide to relax rectal and uterine walls
Flunixine meglumine to minimise PGF2alpha release as a result of trauma to the uterus

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30
Q

What are some DDx for infertility in the mare? (8)

A
  1. True temporary anoestrus
  2. True permanent anoestrus
  3. Ovarian tumour
  4. Irregular oestrus cycle
  5. Endometritis
  6. Silent oestrus
  7. Retention of endometrial cups
  8. Transitional oestrus
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31
Q

What is the most common ovarian neoplasia in mares? What are some DDx?

A

Granulosa theca cell tumour
DDx:
- teratoma
- ovarian haematoma

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32
Q

What are the two most commonly isolated bacteria in cases of equine endometritis?

What are some other non-bacterial causes?

A

Streptococcus equi sp. zooepidemicus
E. coli

iodine/ antibiotics, air, urine, idiopathic

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33
Q

Dioestrus in mares is characterised by compromised defences. What does this include?

A
  1. Decreased immune functions
  2. Closed cervix prevents drainage
  3. No flushing effect
  4. decreased muscle contractions
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34
Q

What are the three main barriers involved in reproductive defence?

A
  1. Vulva
  2. Vestibulo-vaginal sphincter
  3. Cervix
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35
Q

When should samples be taken to test for endometritis?

A

In dioestrus (when cervix is still open)

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36
Q

What is endometrosis?

What about endometrial cysts and transluminal adhesions?

A

Endometrosis: irreversible damage of functional glandular tissue
Endometrial cysts= lymphatic cysts
Transluminal adhesions= end point of EM fibrosis

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37
Q

What are some drug options available for you to treat endometritis?

A
  1. Polyenes
  2. Imidazoles
  3. Triazoles
  4. Lufenuron
  5. Dilute vinegar solution
  6. Dilute providone-iodine solution

(Follow up with OT)

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38
Q

WHAT is it? WHERE is it? HOW do you treat? SPECIFICS?

Melanoma

A

WHAT: mass of melanin-forming cells
WHERE: Ventral tail, anus, perineum, external genitalia, parotid region, oeriocular region, udder and lips
HOW: surgical excision/ debulking, cimetidine, cisplatin, melanoma vaccine
SPECIFICS: grey horses (benign)

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39
Q

What is cimetidine?

A

Histamine H2 receptor antagonist

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40
Q

WHAT is it? WHERE is it? HOW do you treat? SPECIFICS?

Sarcoids

A

WHAT: fibroblastic tumours; non regressing; locally invasive
WHERE: anywhere
HOW: complete excision, caustic ointments, 5-FU, immunotherapy, chemotherapy, BCG
SPECIFICS: bovine papilloma virus 1 and 2. Dx by biopsy

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41
Q

WHAT is it? WHERE is it? HOW do you treat? SPECIFICS?

SCC

A

WHAT: tumours of skin
WHERE: Unpigmented skin (third eyelid, periorbital area, nose and genitalia)
HOW: Surgical excision and adjunctive therapy.
SPECIFICS: UV exposure

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42
Q

WHAT is it? WHERE is it? HOW do you treat? SPECIFICS?

Eosinophilic granuloma (nodular necrobiosis)

A

WHAT: non-tumour nodular skin disease. Smooth nodules, non-pruritic, haired and firm
WHERE: neck, withers, and dorsal trunk
HOW: Sub-lesional corticosteroid injection, triamcinolone, oral prednisolone or surgical excision
SPECIFICS: Insect hypersensitivity possibly

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43
Q

What are some DDx for ulcerated lesions on the distal limb of a horse?

A 
Pythiosis
Habronemiasis
Nodular sarcoids
SCCC
Exuberant granulation tissue
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44
Q

What is pythiosis?

A

Protozoal disease caused by Pythium insidiosum. Aka swamp cancer or kunker. Causes a rapidly growing ulcerated lesion that develops areas of necrosis and fistualae when there is a break in skin integrity

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45
Q

How do you treat cutaneous habronemiasis?

A

Ivermectin (+/- CSs)

Insect repellant and disposal of manure

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46
Q

What are three conditions for dermatophilosis? Where does it usually occur?

A

Moisture
skin abrasions
a carrier animal

aka rain scald or greasy heel

Dorsum, and face (rain exposed areas)

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47
Q

How might you treat folliculitis. furunculosis?

A

Mild cases might not need treatment. Horses can be washed with chlorhex scrub or malaseb. Severe cases may need penicillin G or trimethoprim silfa

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48
Q

How do you dx ringworm in horses? What is the aetiological agent?

A

Trichophyton equinum and mentagrophytes and microsporon equinum.

Microsc. examination of hair shafts, skin scrapings +/- fungal culture (woodlamps not useful)

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49
Q

What breeds are predisposed to pastern dermatitis?

A

Draft/ feathered breeds

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50
Q

What is the typical age of onset of culicoides hypersensitivity? How might you treat it?

A

2-4 years (there may be a hereditary component)
Tx:
-insect repellants
-rugs/hoods
-keeping horses indoors (need ultrafine mesh)
-fans

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51
Q

What causes cutaneous onchocerchiasis? How does it spread? What may be used to treat it?

A

Filarial dermatitis caused by the microfilariae of Onchocerca cervicalis (hypersensitivity reaction). Infection transmitted between horses by Culicoides species.
Tx is with ivermectin or moxidectin

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52
Q

Where are the following lice more likely to cause lesions in horses?

  • Damalinia (Bovicola) equi
  • Haematopinus asini.

How are these treated?

A

D. equi- body
H. asini- base of mane and tail

Ivermectin (and mxi) for suscking lice
Fipronyl and pyrethroid sprays

(give 2-3 treatments 2 weeks apart in order to kill emerging nymphs and adults bc these tx dont kill eggs)

Imadacloprid only needs to be given once

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53
Q 
Where do the following mites cause disease?
Chorioptes bovis (state 3 things about this)
Psoroptes equi
Sarcoptes scabei var equi (state 2 things about this)
A

Chorioptes bovis= leg (sometimes perineum).
-More common in winter. Draft breeds predisposed. Mites may survive many weeks off the host.

Psoroptes equi= body mange/ ear mites.

Sarcoptes scabei var equi= head mange. Starts on head and ears but spreads. Burrows deep

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54
Q

How can you treat mange in a horse?

A

Ivermectin or moxidectin every 2 weeks for 2-3 treatments

Topical tx:
fipronyl (once a week for a month)
lime sulphur

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55
Q

What is urticaria? What is the gold std for testing?

A

Transient focal swellings= hives= wheals
Result from dermal oedema arising from vasodilation (not always itchy)

Intradermal skin testing

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56
Q

What drugs commonly cause urticaria?

A

Penicillin, sulfa drugs, NSAIDs, and phenothiazines

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57
Q

How can atopic skin disease be treated in horses?

A 
Management of environmental conditions
CSs (dex, pred)
Antihistamines (not v useful)
Hyposensitization
Avoiding exposure!!
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58
Q

How might you treat bullous keratopathy?

A
  1. Cover cornea (temporary tarsorrhaphy)
  2. Keratectomy (debride devitalised cornea and conjunctival flap/ graft)
  3. Topical A/bs, anti-inflammatories
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59
Q

What are some chronic signs of uveitis? (8)

A
  1. Phthisis bulbi (shrunken, non-functional eye)
  2. Cataract formation
  3. Posterior synechia (iris adheres to the lens)
  4. Retinal detachment
  5. Hyperpigmented iris
  6. Vitreous opacity
  7. lens luxation
  8. Glaucoma
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60
Q

How much is too much blood loss in a horse?

A

8L/500kg

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61
Q

What is tranexamic acid?

A

It’s an anti-fibrinolytic used to control excessive bleeding

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62
Q

What are some warning signs for avascular necrosis in the distal limb?

A

Severe lameness 2-3 days

coronary band serum

63
Q

How might you stabilise fractures of the:

  • distal metacarpus and below
  • mid-metacarpus to distal radius
  • mid to proximal radius
  • mid to proximal tibia
A
  • distal metacarpus and below: commercial splint or padded heavy bandage with splint dorsally in FL or plantarly in HL + cover with cast material
  • mid-metacarpus to distal radius: RJ bandage, 2 splints, elbow to ground, lateral and caudal
  • mid to proximal radius: RJ bandage, lateral splint
  • mid to proximal tibia: RJ bandage, board on lat aspect
64
Q

What is proud flesh? What causes it and what is the problem with it?

A

Excessive granulation tissue
Chronic infection, chronic inflammation
Prevents contraction and epithelialisation

65
Q

What is a differential diagnosis for proud flesh? in which areas would you not expect this and why?

A

Sarcoid/ SCC transformation

Wouldnt expect on proximal limb bc injuries genrally heal well proximally

66
Q

What is a sequestrum?

A

Area of infected avascular bone (wound may strip off periosteum)

67
Q

How long does it take for a pinch/ punch graft to take?

A

10 d

68
Q

How long do you need to allow for nerve blocks of the:

  • distal limb
  • proximal limb
  • intraarticular
A
  • distal limb: 10- 30 mins
  • proximal limb: 20-40 mins
  • intraarticular: 5-10 mins
69
Q

What are the three presentations of osteochondrosis? Give examples.

A
  1. Flap and fragment formation= occur at margin of wt bearing and non-wt bearing cartilage (eg. trochlear ridges, sagittal ridge of MC/MT3)
  2. Fragmentation alone= non weight bearing areas (eg. distal intermediate ridge of tibia, proximal plantar P1 fragments)
  3. Subchondral bone cyst= weight-bearing areas (eg. medial condyle of femur, med prox radius, glenoid. PIPJ)
70
Q

What is the pathogenesis of OCD? What are some predispositions?

A 
Weak bone and cartilage subjected to excessive forces (multifactorial: genetic, dietary, exercise). Retained cartilage, flap and fragment formation
Predispositions:
-large breeds (WBs, TBs)
-high CHO intake
-mineral imbalances (Cu def, Ca:P)
71
Q

What is a subchondral bone cyst? Where are some common sites that they occur?

A

Secondary change following injury to cartilage or subchondral bone.

  1. Stifle
    - medial condyle of the femur
  2. Elbow
    - Medial proximal radius
  3. Shoulder
    - glenoid
  4. Pastern
72
Q

What are some tx options for equine OCD?

A 
Conservative tx (restrict exercise, restrict diet, monitor radiographically)
Surgical tx (removal of fragments, debridement of subchondral cystic lesions)
73
Q

Where is the most common site for OCD in a horse? How may OCD at this site be treated?

A

Tarsus-> tarsocrural swelling

DIRT (distal intermediate ridge of tibia) lesions-> arthroscopy
Lateral trochlear ridge lesions-> lytic lesions should be treated conservatively; flaps or fragments treated with arthroscopy

74
Q

How is fetlock OCD often treated?

A

Conservatively. Often an incidental finding. Arthroscopy if fragment is present.

75
Q

In what age horses does shoulder OCD often present in?

How is is treated?

A

2 year olds. Sig degen changes present when diagnosed.

Arthroscopy is tx of choice but poor px (50% success rate)

76
Q

What blocks are available to do in the equine hindlimb?

A 
Regional: 
-subtarsal
-tibial and peroneal
Intra-articular:
-tarsometatarsal
-centrodistal joint
-tarsocrural joint
77
Q

What radiographic views are necessary when assessing the tarsus?

A

A minimum of 4 views needed:

  1. LM
  2. Dorsoplantar
  3. DL plantaromedial oblique
  4. DM plantarolateral oblique
78
Q

What is bone spavin?

How is it treated?

A

Bone spavin is a bony growth (osteoarthritis) within the lower hock joint of horse (or cattle). It is an overdiagnosed condition in which radiographic changes are unreliable and in which diagnostic analgesia must be used.

Tx: Phenylbutazone, intra-articular corticosteroid, arthrodesis

79
Q

What are common sites affected with OCD in horses?

A
  1. Tarsus
    - distal intermediate and lateral trochlear ridges
    - medial malleolus
  2. Stifle
    - lateral and medial trochlear ridges
    - patellar
    - medial condyle of femur
  3. Fetlock
    - Sagittal MC3 ridge
    - ununited palmar/plantar surface
  4. Shoulder
    - humeral head
    - glenoid cavity
  5. Elbow
    - medial proximal radius
80
Q

What are some ddx for lameness in a young horse?

A

Developmental conditions, sepsis, trauma, foot abscess, OCD

81
Q

Where might distension of the distal interphalangeal joint

dorsal pouch be observed or palpated?

A

Dorsal aspect of coronary band

82
Q

A horse that presents lame and which has more severe lameness when lunged or on a hard surface likely has lameness in which area?

A

Pastern or foot

83
Q

Which regional and intra-articular nerve blocks are available for the pastern?

A

Regional:

  • Palmar digital nerve block
  • Pastern ring block
  • Abaxial nerve block

Intra-articular:

  • Distal IPJ
  • Proximal IPJ
84
Q

What is low ringbone and what is it often associated with?

A

Osteoarthritis with associated periosteal bone production on phalanges in this distal IPJ.
Not common and often associated with intra-articular fractures or collat lig injury.

85
Q

What is high ringbone? in which cases is it seen?

A

Osteoarthritis with associated periosteal bone production on phalanges in this proximal IPJ.

Causes chronic low grade lameness and seen in young horses with subchondral cystic lesions or fractures, and older horses with chronic degenerative condition

86
Q

What steps might you go through to diagnose high ringbone?

A 
Diagnostic analgesia (nerve blocks)
Radiographs may be unreliable unless the condition is advanced. May help identify fractures or cysts though
Scintigraphy
87
Q

What is proximal suspensory desmitis?

A

The term proximal suspensory desmitis (PSD) is restricted to lesions confined to the SL in the proximal one-third of the metacarpus

88
Q

What nerve blocks are available for the fetlock?

A

Regional:
-Abaxial (may block sesamoids)
-Low 4 point (lat/med palmar nerves + lat/med palmar metacarpal nerves)
Lameness localized to fetlock if pastern ring block negative and low 4-point block positive

Intra-articular:
-Needle passed through the collateral ligament of sesamoid with the joint
flexed

89
Q

What radiographs views might be needed to assess fetlock pathology?

A

-LM
-DP - elevate 10°
-Obliques
– Elevate 10° forelimbs
– Elevate 35° hind limbs
-Flexed LM

• Views to highlight plantar aspect of condyle
– Elevated oblique
– DP with leg forward

90
Q

What are common sites of subchondral bone injury in the fetlock?

A

Lateral condyle in HLs

Medial and lat condyles in FLs

91
Q

What is recommended tx for subchondral bone injury in the fetlock?

A

3 months rest

92
Q

What are the synovial structures of the equine carpus?

A
  1. Antebrachiocarpal joint
  2. Midcarpal joint
  3. Carpometacarpal joint
  4. Carpal sheath
  5. Extensor tendon sheaths
93
Q

The carpus is commonly injured by high speed exercise. What are the highest anatomical areas of loading?

A
  1. Midcarpal joint (radial carpal bone and radial facet of third carpal bone)
  2. Antebrachiocarpal joint (distal radius and int carpal bone)
94
Q

Failure of subchondral bone in the carpus to adapt to increased stress may lead to what?

A

Subchondral bone necrosis
Chip fracture
Slab fracture (extends from one articular surface to another)

95
Q

What is the most common fracture of the carpus?

A

Frontal slab fracture of the radial facet of the third carpal bone, followed by fractures of the intermediate facet and both facets of this bone.

96
Q

Swelling over the dorsal aspect of the carpus may involve what structures? What about over the lateral aspect?

A
  1. Antebrachiocarpal joint
  2. Midcarpal joint
  3. Extensor tendon sheaths
  4. Subcutaneous

Lateral:

  1. Carpal sheath
  2. ABC joint
97
Q

Carpal joint pain (including fractures) is painful on flexion. True or False?

A

True

98
Q

What nerve blocks are available for the carpal area in a horse?

A

Regional: Subcarpal, median and ulnar block

Intra-articular: midcarpal joint, ABC joint

99
Q

What are the minimum four radiographic views necessary for assessment of carpal pathology?

A
  1. Flexed LM
  2. DL palmaromedial oblique
  3. DM palmarolateral oblique
  4. Skyline of 3rd carpal bone
100
Q

In the carpus, anything greater than a mild lameness usually indicates significant pathology. True or False?

A

True

101
Q

What are the synovial structures of the shoulder joint?

A

Bicipital bursa

Shoulder joint

102
Q

What is characteristic of shoulder lameness?

A

Shortened cranial phase of stride (+/- muscle atrophy)

103
Q

What nerve blocks are available for the shoulder joint?

A

Intra-articular injection of shoulder joint

Intra-thecal injection of bicipital bursa

104
Q

What are some common conditions of the shoulder joint?

A
  1. OCD
  2. OA
  3. Supraglenoid tubercle fracture
  4. Bicipital bursitis
105
Q

How might an ulnar fracture present? What other conditions might affect the elbow joint?

A

Dropped elbow. (common paddock injury)

Subchondral cystic lesions (which can be identified on scintigraphy images)

106
Q

Elbow physeal fractures in foals re often repairable with tension band plates. Does this treatment have a good prognosis?

A

Yes- about 70% return to athletic function

107
Q

What are the synovial structures of the metacarpus?

A

Carpal canal and digital sheath

108
Q

What are common pathologies of the metacarpus?

A

Periostitis
Stress fracture
Osteomyelitis

109
Q

Tendon injuries in the distal forelimb often cause significant lameness no matter how significant they are. True or False?

A

False. Lameness more often than not indicates significant tendon injury

110
Q

What might mild and more severe lameness indicate with respect to SL injuries?

A

Mild lameness: branch lesions, FL body lesion
Severe: Prox SL, HL body* lesions

**body of SL

111
Q

What blocks are available to test pathology of the SL?

A

Subcarpal/ tarsal block followibg low 4 point
Ulnar or tibial block
Perineal block.

Note, diagnostic analgesia is rarely needed if swelling is present

112
Q

An intra-articular midcarpal block may localise pain to the carpus or where else?

A

Proximal suspensory lig

113
Q

What radiographic view would you use to assess the splint bones of the metacarpus?

A

DM lateral oblique to see lateral splint bone and vice versa

114
Q

Is SDF tendonitis more commonly a problem of the forelimb or hindlimb? What is its pathogenesis?

A

FL. High recurrence rate (at junction of normal and repaired tendon)
Path: Ltd collagen turnover in adult tendon-> fatigue failure of collagen fibres occurs with repetitive loading. Once damage occurs, Type I collagen is replaced with type II and the fibre arrangement becomes poorly aligned-> increased tendon cross sectional area

115
Q

What are some options for the treatment of SDF tendonitis?

A
  1. Rest, anti-inflammatories, controlled exercise program
  2. Superioir check ligament desmotomy (increases chance of SL failure)
  3. Stem cells
  4. Platelet rich plasma
  5. Shockwave therapy
116
Q

Body and branch suspensory lig desmitis predominantly occurs in __________. in the ____limbs. Clinical signs include _______, _________, and ________ (variable). The prognosis for SL desmitis is _______.

A

TBs and SBs
FL (TBs) and FLs/HLs (SBs)
Pain, swelling and lameness
Poor in Tbs and fair in SBs

117
Q

Proximal suspensory desmitis occurs in _______. It may occur in the FL or HL, but px is poorer in the ____. Some treatment options include ________.

A

all types of horses
HL
3 months rest, shockwave therapy, fasciotomy and neurectomy or stem cells

118
Q

The amount of splint bone that may be amputated as a treatment for splint bone fractures varies between limbs and aspects. Identify these differences.

A

MetaTARSAL 4- whole bone
MetaCARPAL 2- distal half
All others, distal 2/3s

Why? Removal of greater amounts requires stabilisation of proximal fragment

119
Q

Where do flexural deformities often occur?

A

-foot
-pastern
-fetlock
-carpus
Club foot= flexural deformity of the coffin joint

120
Q

What are some examples of congenital flexural deformities and angular deformities?
What about some examples of acquired deformities?

A 
Flexural (muscle contracture reflexive to s pain source):
-tendon laxity
-limb contracture
Angular (arises from physis):
-ligament laxity
-poor bone dvpt
ACQUIRED
Flexural:
-limb contracture
-ruptured extensor tendons
Angular:
-growth plate abnormalities
121
Q

In regards to congenital angular limb deformities, seeing if the leg can be manually straightens gives us what indication?

A

Indicates whether bone growth abnormality or ligament laxity. If bone problem, then it wont be able to straighten.

122
Q

How would you manage poor bone ossification in the tarsus or carpus?

A

Confine, provide support through splints or casts. Weight bearing will lead to disintegration of cartilage/ bones

123
Q

How would you manage an angular deformity from growth plate?

A
  • Confine and reduce weight bearing
  • Maintain foot balance (lateral/ medial extension may be needed on side that we want limb to deviate to)
  • Sx (periosteal strip-> growth acceleration; Bridge growth plate -> growth retardation)
124
Q

What are some indications for surgery when assessing:

  • Carpal angular deformities from growth plate
  • Fetlock angular deformities from growth plate
A

Carpus:

  • severe deformities
  • not improving with confinement
  • Over three months of age
  • 8-20 degree-> periosteal strip
  • > 20 degree-> physeal bridge
  • > 25 degree= guarded px

Fetlock:

  • severe deformities
  • From 2 weeks of age (and >30days)
  • 5-8-> periosteal strip
  • > 8 physeal bridge
  • > 12= poor px
125
Q

How do you manage congenital flexural deformities in foals? How about if it is acquired?

A

Weight bearing
Tetracyclines-> tendon relaxation
Sx if fail to respond

Acquired: treat cause, phenylbute, tetracyclins, sx

126
Q

How do you tx carpal flexural deformities? How about pastern?

A

Splinting
desmotomy of FCU and UL

Splinting + inferior check lig desmotomy

127
Q

How do you diagnose septic arthritis in foal?

How do you treat?

A 
Synovial fluid analysis:
Total WCC>10 x 10^9/L
Protein >25g/L
Neutrophils >90%
(then look at radiographs for subchondral or physeal involvement)

Tx: treat any FPT, broad spec A/bs, lavage joint space, debride affected bone (if fibrin or bone lysis)

128
Q

How many components are there in each segment of the spine?

A

Cervical- 7
Thoracic- 18
Lumbar- 6

129
Q

The sacroiliac joint has both hyaline and fibrocartilage. True or False? What ligaments connect the sacroiliac joint?

A

True. Sacrum- hyaline, Ilium- fibrocartilage

Dorsal, interosseous and ventral

130
Q

What are some clinical signs of pain in the longissimus muscle?

A

Stiffness in TL spine

Inability to perform at fast paces

131
Q

What should comprise your clinical exam of a horse presenting with stiffness and back pain?

A

Observation of muscle mass and symmetry (tuber sacrale)
Palpation of dorsal spinous processes, muscles and tuber sacrale
Examine limbs- examine for lameness, lunge at canter, maybe with rider
Nerve blocks? Dorsal spinous processes, sacroiliac region (dorsal SI ligament- local infusion; regional; peri-articular)
+/- radiographs (DSPs, facet joints)
+/- US (spinal ligs, SI ligs)

132
Q

Where are the two major areas of sacroiliac pain? In which horses is it most common? What are some signs of it? What are some Ddx? What are some tx options?

A
  1. Dorsal sacroiliac ligaments and insertions
  2. SI joints
    (Pain on palpation of tuber sacrale-> dorsal SI lig injury or ilial stress fracture)

Older horse, Larger horses, WBs

Restricted HL impulsion, most obvious when ridden; poor TL muscle development, HQ asymmetry, straight HL flight, restricted TL flexibility, pain on pressure over tuber sacrale, reluctant to stand on one HL for too long

DDx: Bilat HL lameness, TL spine pain, pelvic fracture, exertional rhabdomyolysis

Tx: rest, controlled exercise amd NSAIDs for acute case. Periarticular injection of CSs, bute, unridden exercise and shockwave therapy for chronic cases

133
Q

What are some clinical findings of overriding dorsal spinous processes? What are some tx options?

A

Poor performance, reduced muscle mass, reduced flexion/ extension of the spine.
(Need to block to find out significance)
Rest, local CS injection, surgical resection

134
Q

What are the different types of rhabdomyolysis?

A
  1. Non-Exertional
  2. Exertional
    - Sporadic exertional rhabdomyolysis (normal muscle function)
    - Chronic exertional rhabdomyolysis (underlying abnormality in muscle function)
    * recurrent exertional rhabdomyolysis
    * polysaccharide storage myopathy
135
Q

What are some causes of non-exertional rhabdomyolysis?

A
  1. Inflammatory or Infectious
    - Bacterial (clostridium spp, Streptococcus equi, Salmonella)
    - Viral (Equine influenza virus, Equine herpesvirus 1)
    - Parasitic (sarcocystis fayeri)
  2. Nutritional
    - Vit E or Selenium def
  3. Toxicities
    - Ionophores
    - Coffeeweed, white snakeroot and marshmallow weed
  4. Traumatic
136
Q

What is sporadic exertional rhabdomyolysis? What are inciting/predisposing causes?

A 
1-2 episodes, no intrinsic muscle abnormality
Numerous pre-disposing factors such as:
1. Over-exertion
2. Excessive dietary soluble CHO
3. Temperament
4. Concurrent illness
5. Electrolyte imbalances
6. Hormonal influences
7. Vit E and selenium def
137
Q

What is chronic exertional rhabdomyolysis? What are inciting/predisposing causes?

A

repeated episodes which significantly affect athletic performance= intrinsic muscle abnormality

  1. Excessive dietary soluble CHO
  2. Temperament
  3. Electrolyte imbalances
  4. Hormonal influences
  5. Vit E and selenium def
138
Q

What are the two main forms of chronis exertional RM?

A
  1. Recurrent exertional rhabdomyolysis= mechanism of disease unknown. Maybe related to muscles calcium handling. Occurs mostly in young TB, SB and arabian racing fillies. Incr. sensitivity to caffeine, halothane and K. Tx with dantrolene
  2. Polysaccharide storage myopathy= abnormal accumulation of glycogen in the muscle. Most common in QH and QH types (draft and WBs). Result of increased glycogen production which is less branched. Mutation in GYS1 gene?
139
Q

What is the significance of the GYS1 gene?

A

encodes enzyme glycogen synthase. This enzyme activity is increased in horses with this mutation. mutation found in horses with polysaccharide storage myopathy

140
Q

How can equine rhabdomyolysis be diagnosed?

A
  • PE
  • Serum/plasma biochem (AST, CK, LDH)
  • myoglobinuria?

(if chronic case…)

  • exercise challenge
  • urinary fractional excretions
  • muscle biopsy
141
Q

What are some ddx for sporadic exertional rhabdomyolysis?

A

Colic, pelvic fracture, laminitis, neurological disease

142
Q

What might be some diagnostic indicators of Polysaccharide storage myopathy?

A
  1. Elevated AST, CK, LDH
  2. Genetic mutation in GYS1 gene (hair root or blood sample)
  3. Muscle biopsies with subsarcolemma vacuoles, increased PAS-positive staining for muscle glycogen or amylase resistant abnormal crystalline polysaccharide inclusions
143
Q

What is the px of exertional rhabdomyolysis? What are some potential consequences if tx isn’t provided?

A

Sporadic ER-> excellent px
Chronic ER-> limits athletic performance

Continued exercise might lead to permanent muscle damage and acute renal failure (as myoglobin and haemoglobin are both nephrotoxic)

144
Q

How might you treat exertional rhabdomyolysis?

A

If severe, acute:

  • IV fluids (for dehydration and provide diuresis)
  • Manage pain (watch for GIT stasis!)

If chronic:

  • Manage/ eliminate trigger factors
  • Diet (reduce CHO)
  • exercise daily in set routine
145
Q

What are some useful biochemistry markers in assessing inflammatory processes in horses?

A

Fibrinogen= an APP that takes48-72 hours to increase

Serum Amyloid A= an APP that increases earlier than fibrinogen but may also decrease to normal with chronic inflammation

146
Q

What is the purpose of a rebreathing exam?

A

increases inspired CO2-> increased depth and rate of resp. It accentuates adventitial sounds if present. Also allows assessment of coughing, recovery and tolerance

147
Q

in which cases might you use TTW over BAL or vice versa?

A

TTW: used to collect samples for cytology and CULTURE (not trans-endoscopically though). Good for focal lung disease and allows collection of sample not contaminated with URT commensals

BAL: more sensitive in detecting alveolar pathology and generalised lung disease (opposite to smallies). NOT suitable for culture. Good for detecting infl. diseases of the airways

148
Q

How do you interpret results from a TTW? How about a BAL?

A 
TTW:
Fungal hyphae (a few) is normal
Neutrophils are variable (3 - 50+%)

BAL:
Neutrophils <5%, eosinophils <0.5%, mast cells < 2%, remainder is macs and lymphocytes
Infl airway disease= Increased amounts of neuts, eosinophils or mast cells
Recurrent airway obstruction (Heaves) is usually >25% neutrophils

149
Q

Besides radiography, US, what are other diagnostic tools useful in assessing respiratory disease?

A 
BAL (not good for culture)
TTW
Nasopharyngeal swabs
Culture of abscessed LNs
Sinucentesis
Guttural pouch aspirates
CT

Thoracocentesis- essential for pleuropneumonia
Lung biopsy
(these latter two are for LRT)

150
Q

What are some Ddx for Hendra?

A
  1. Plant poisonings
  2. Ionophore toxicity
  3. Intestinal lesions
  4. Bacterial pneumonia
  5. Viral encephalitis
  6. Pupura haemorrhagica
  7. Snake bote envenomation
  8. Paralysis ticks
151
Q

In which animals and under which conditions is EHV-1 and 4 most commonly seen?

A

Most frequently in weanlings, yearlings and young adults

Most often after entry into a racing stable (mixing, stress…etc)

152
Q

What is purpura haemorrhagica?

A

A complication of strangles that involves a type 3 hypersensitivity reaction (immune complex mediated)-> vasculitis. It leads to severe lib oedema (-> skin sloughing), petechiation or ecchymosis an/or glomerulonephritis. Treated with CSs and penicillin

153
Q

What is Bastard strangles?

A

A complication of strangles infection that results in lymph node abscessation in parts of the body other than the URT.

DVM3 (13 decks)

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