EBCM Exam One Flashcards
(186 cards)
1
Q
If you note a conformational abnormality upon examination of a horse, what should your first next step be?
A
(Reposition the horse to make sure it is a true conformational abnormality)
2
Q
What portion of the hoof should be trimmed in a foal with pigeon-toed conformation?
A
(The medial wall should be mildly lower)
3
Q
What portion of the hoof should be trimmed in a foal with a splay-footed confirmation?
A
(The lateral wall should be mildly lower)
4
Q
What other conformational abnormality is typically paired with a pigeon-toed conformation?
A
(Base-narrow)
5
Q
Horses with a base-wide conformational abnormality typically overload which aspect of their lower limb and foot?
A
(The medial aspect, they land on the inside of their foot; exact opposite for base-narrow → lateral aspect/outside of foot)
6
Q
Is varus or valgus described as a lateral deviation from the normal forelimb plumb line?
A
(Valgus; varus is medial deviation from the normal forelimb plumb line)
7
Q
Does a knock-kneed or bow-legged/bandy-legged horse result from a foal with carpal varus?
A
(Bow-legged)
8
Q
What is indicated if you observe sickle hocks in a foal?
A
(Incomplete ossification of the tarsal cuboidal bones, the crushing that results can lead to sickle hocks in foals so should radiograph them)
9
Q
What are horses with a splay-footed conformation predisposed to due winging in when in motion?
A
(Interference or kicking their own legs)
10
Q
What conformational abnormality is commonly seen in foals at birth but will disappear by 3 months of age but can also be acquired in jumpers?
A
(Dorsal deviation of the carpus aka buck-kneed, sprung knees, hanging knee, goat knees, or over at the knee)
11
Q
(T/F) Mild outward rotation of the hindlimbs in a horse is normal.
A
(T)
12
Q
A cow-hocked horse (excessive outward rotation of the hocks) will often have what other conformational abnormality?
A
(Base narrow)
13
Q
Horses with a toed-in conformation will wing in/out (choose)?
A
(Out)
14
Q
Horses with a toed-out conformation will wing in/out (choose)?
A
(In)
15
Q
What two characteristics of the trauma causing a fracture determines the configuration of a fracture?
A
(The direction and amount of force associated with the causing trauma)
16
Q
(T/F) You should place a splint on a suspect fracture prior to taking field radiographs.
A
(T)
17
Q
(T/F) A distal limb fracture should always be splinted.
A
(T)
18
Q
If you are placing a splint on a patient with a fracture anywhere from the distal quarter of the cannon bone to the coronary band in a forelimb, where should the splint extend to and from?
A
(Should extend from the toe to just below the carpus)
19
Q
If you are placing a splint on a patient with a fracture anywhere from the distal quarter of the radius to mid cannon bone, where should the splints extend to and from?
A
(Elbow to floor, 2 splints one caudal and one lateral)
20
Q
Why must a splint placed for a mid to proximal radius fracture extend from the ground to the withers?
A
(When the horse uses the limb, the muscles in the proximal forelimb will abduct the limb instead of their normal movement due to the incomplete bony column; splint needs to extend past the joint above and below to attempt to mitigate that effect)
21
Q
What are three differentials if you are presented with a horse with a dropped elbow?
A
(Radial nerve injury, olecranon fracture, humerus fracture → can place a caudal splint)
22
Q
When splinting a rear limb with a fracture anywhere from the distal quarter of the cannon bone to the coronary band, the splint is placed on the dorsal/plantar (choose) side.
A
(Plantar)
23
Q
Optimally, though not always possible, when transporting a horse with a fracture, the limb with the fracture should be placed at the front/rear (choose) of the trailer.
A
(Rear → if a hard brake occurs, the horse will shift forward and onto which ever legs are at the front)
24
Q
What are the two steps to the formation of osteochondrosis?
A
(Failure of vascular invasion of the cartilage template and then there is not enough blood supply for that cartilage to then ossify into bone so it’s a failure of vascular invasion followed by a failure of ossification)
25
Horses with OCD are typically slow growing and small/rapidly growing and large (choose).
(Rapidly growing and large)
26
An excess/deficiency (choose) in energy provided through diet is strongly implicated as a cause of OCD.
(Excess)
27
An imbalance in what two trace minerals is thought to be a possible cause of OCD?
(Too little copper or too much zinc)
28
Do subchondral bone cysts occur in areas of gliding or weight bearing?
(Weight bearing, dissecans lesions occur in gliding areas)
29
What are two reasons you should not use steroids in cases of OCD?
(It can cause ossification of structures that should not be ossified and you don’t want steroids in the joint if you happen to need to go to surgery)
30
(T/F) A joint with OCD will always have effusion.
(F, most will but some will not especially joints closer to the body)
31
Flexion/extension (choose) of a joint with OCD will worsen lameness.
(Flexion, due to the effusion usually present and putting further pressure on the joint capsule)
32
Why may there still be lameness present after blocking a joint with a subchondral bone cyst?
(Because the block can’t block out the bone pain associated with SBCs)
33
What are two reasons to not immediately jump to surgical correction of OCD/SBC in foals?
(One → they may be able to heal it themselves with time, make sure to monitor/document/radiograph through 18 months of age to ensure proper healing; two → foal bone is much softer than adult bone and that can make discerning the border between normal bone and bone with malacia more difficult)
34
Debrided OCD beds heal with what type of cartilage?
(Fibrocartilage, not the normal hyaline cartilage found in joints)
35
What is the minimum amount of time a horse needs to be stall rested post OCD surgery?
(60 days, no turnout, then gradual return to work)
36
Why is the rehabilitation period longer for subchondral bone cysts corrected by surgery compared to OCD?
(Because SBCs are related to weight bearing surfaces whereas OCD are gliding surfaces)
37
What main pathology being present along with an OCD lesion or SBC decreases the prognosis?
(Osteoarthritis)
38
Bilateral OCD lesions occur in about 50% of cases, so you should take radiographs of the contralateral joint. You take a radiograph of a contralateral joint and do not see any changes, can you stop there?
(No, if only the cartilage is sheared off, you will not be able to tell if there is an OCD lesion, further testing (flexion tests, IA blocks, etc.) is warranted especially if lameness noted on contralateral limb)
39
If a horse has multiple joints with OCD lesions, where else should you check for OCD?
(Their neck)
40
OCD/SBC (choose) is very common in the femoropatellar joints.
(OCD, SBC uncommon)
41
OCD lesions of the lateral/medial (choose) trochlear ridge in the femoropatellar joint are much more common.
(Lateral)
42
If you find OCD lesions on the trochlear ridges of the femoropatellar joint, you should explore what structure for additional lesions?
(The patella, look for kissing lesions)
43
OCD/SBC (choose) is very common in the femorotibial joints
(SBC, OCD uncommon)
44
SBC lesions of the lateral/medial (choose) femorotibial joint are more typical.
(Medial)
45
(T/F) The marginal sclerosis of an SBC lesion may demonstrate its maturity.
(T)
46
OCD/SBC (choose) is very common in the tibiotarsal joint.
(OSD, SBC on trochlear ridges are uncommon)
47
OCD and SBC of the radiohumeral joint is generally less common in horses compared to other joints but they do occur, give the location that either would most likely occur at.
(SBC → medial proximal radial condyle, OCD → distal humeral condyle)
48
(T/F) Surgery is not an option for OCD/SBC of the radiohumeral joint so exhaustive conservative therapy is pursued.
(T, prognosis ain’t great)
49
OCD/SBC (choose) is more likely to affect the femoral head in the coxofemoral joint.
(SBC)
50
What are some things that can impact the rate of growth of a horse's hoof?
(Time of year, pathology, nutrition, and job/exercise level)
51
Why are horse’s hooves trimmed?
(To remove excess length, to remove distortion, to improve the base of support, to prevent chipping, and to remove disease/deteriorated areas)
52
Why do horses wear shoes?
(Protection, treatment, traction, and to alter gait)
53
(T/F) If a horse does not fall into a typical category for why horses wear shoes (protection, treatment, traction, and to alter gait), they should not be shod.
(T, cons outweigh the pros)
54
What are some consequences of horse shoes?
(Increases shock/concussion to the distal limb, traumatic hoof wall loss, puncture wounds from clips/nails, spring/twisted shoe, injury when kicking, nail too close to sensitive structures)
55
What is the main difference in a hoof trim if you are going to put a shoe on or not?
(Shoe → trim shorter, should be flat with a sharp edge, no shoe → outer edge should be rounded to prevent chipping and should be left longer to allow for wearing)
56
What does it mean that you want to achieve a matched hoof pastern axis?
(The dorsal wall of the hoof will match the angle of the bony column of the foot → allows spreading of the load evenly between all structures of the foot)
57
What should the length and angle of the heel be in relation to the dorsal hoof wall in an appropriately trimmed horse hoof?
(Angle should match the dorsal hoof wall and the heel would optimally be about ⅓ the length of the dorsal hoof wall)
58
The frog would optimally extend over what percentage of the length of the hoof?
(60%)
59
(T/F) A positive palmar angle is optimal, average is usually 3-5 degrees.
(T, do not want a flat/negative palmar angle)
60
What is a broken back hoof pastern axis?
(When the angle of P2 and P1 are steeper than P3)
61
What structures are overloaded with a broken back HPA and what conditions can that predispose the horse to?
(Overloaded → DDFT, navicular bone, P2, and P1; conditions → navicular dz, ring bone, coffin joint inflammation, hoof cracks, and sheared heels)
62
What is a broken forward hoof pastern axis?
(When the angle of P3 is steeper than that of P1 and P2 → stresses the suspensory ligament in particular)
63
What is the main positive function of a hoof pad?
(Recruits the sole and frog in load sharing, others → protect and support, align the hoof pastern axis, protect wounds, act as artificial sole depth, aid with shock dissipation)
64
What substance can be added to packing material for a hoof pad that is a good antimicrobial?
(Copper sulfate)
65
Why must silicone be used under a hoof pad?
(Bc it does not bond to the sole)
66
Why is oakum a good option for horses with white line disease and/or abscesses?
(It allows for drainage → is non-sealing)
67
What are some shoe options that can ease breakover?
(Rolled toe, rocker toe, square/blunt toe, and bar shoes)
68
How should a hoof be trimmed to fix a broken back HPA?
(Trim the toe, not the heel; can also use wedges)
69
How should a hoof be trimmed to fix a broken forward HPA?
(Trim the heel, not the toe; should aim to also treat the primary cause if it related to chronic lameness or a flexural deformity)
70
In a wry foot, is the portion of the hoof that rolls under the foot or the portion of the hoof that flares at an increased risk for development of a quarter crack?
(The portion that rolls under the foot)
71
What is the typical etiology for wry feet?
(Base narrow or base wide conformation)
72
You have a wry foot due to a base wide conformation, when shoeing should the shoe be placed with excess shoe on the lateral or medial hoof wall?
(You’ll want excess shoe on the medial hoof wall because that will be the wall that is rolling under in a base wide conformation, flare of the lateral wall should be trimmed)
73
What is the goal for shoeing to fix sheared heels?
(Decreasing the load of the displaced heel)
74
What do flat feet predispose a horse to?
(Sole bruising and subsequent lameness)
75
What are the types of hoof wall rings, which are normal/abnormal, and what causes each type?
(Parallel rings → normal, caused by stress, nutrition, climate or body temperature change, irritating substances on the coronary band; divergent rings → abnormal, caused by systemic or mechanical laminitis and subsequent mismatch in the growth of the heel and toe)
76
How is thrush treated?
(Prevention is the first step, make sure housing is clean and hoof care is appropriate and that the horse does not have any other cause for lameness; for actual foot care → remove affected frog with hoof knife, soak in epsom salts and bandage with betadine soaked gauze, soak/bandage until frog becomes dry and hard then apply 7-10% iodine tincture until adequate regrowth has occurred)
77
You are presented with a horse that has abnormal hypertrophic horn tissue growing on its frog that has foul-smelling exudate, what is the horse’s issue and how can you treat it?
(Canker, radical debridement of the horn tissue and bandage with 10% benzoyl peroxide in acetone and metronidazole powder → can be very difficult to tx)
78
How does lameness result from keratomas?
(Pressure of the tumor on P3 or bacterial penetration around the keratoma resulting in subsolar abscessation)
79
What substance of the hoof is targeted by fungi and bacteria that invade minor hoof wall separations/defects and cause progressive hoof wall destruction/separation characterizing white line disease?
(Keratin)
80
What does the lay term sidebone mean?
(Ossification of the collateral cartilages)
81
What does the lay term quittor mean?
(Chronic infection and necrosis of collateral cartilages of P3)
82
Why do tendons still need some load when healing from injury?
(Tendon cells can both be overloaded or underloaded, overloading obviously leading to injury of the cells and apoptosis but also not having any tension on the cells can trigger them to apoptose and release collagenases)
83
What is a simple way to reduce excessive compression of a healing tendon?
(If it is caused by a retinaculum, cut the retinaculum)
84
(T/F) Extensor tendon injuries are associated with a good to excellent prognosis regardless of the type of injury and can heal with rest, without intervention.
(T)
85
What is the classic appearance associated with peroneus tertius rupture in horses?
(Flexed stifle and straight hock, should not be possible with an intact peroneus tertius)
86
Is tendinitis of the SDFT or the DDFT more common?
(SDFT)
87
Why do SDFT tendonitis lesions tend to be core lesions?
(Hyperthermia of the core tenocytes (though they are more heat resistant, enough heat can still injure them) and less crimp to the internal aspect of the tendon (increased tension on the collagen fibrils central to the tendon))
88
Are older or younger horses more likely to experience SDFT tendonitis?
(Older, tendons remodel as small injuries occur but as the horse gets older, tendons have a more difficult time maintaining themselves)
89
What do you expect to feel on palpation of a tendon experiencing tendonitis?
(Changes in diameter (fresh injuries will feel gelatinous and chronic injuries will feel firm) and resistance to squeezing of the tendons)
90
The first two weeks of healing a tendon injury should be focused on what concepts?
(Decreasing inflammation and compression)
91
When can controlled exercise begin in the care of tendon injuries?
(2 weeks, hand walking only, this is also when you can decide between medical and surgical tx)
92
Why should horses be stall rested for 2 days post extracorporeal shockwave therapy?
(Because shockwave causes analgesia, horse will feel better and can reinjure themselves)
93
What are some of the effects of extracorporeal shockwave therapy?
(Bone microfractures and hematoma that leads to osteoblastic activity and healing (currently not studied if it does this to tendons as well but it is thought to), analgesia through myelin sheath disruption, and induces neovascularization (speeds healing))
94
If a horse with a tendon injury has healed and is sound, they can gradually increase to full work starting at what time period after the initial injury?
(6 months, tendon takes 18 months to remodel so even after that 6 months, should still keep a close eye on them)
95
You should not start trotting a horse with a tendon injury until what has resolved on ultrasound of the tendon?
(Any anechoic areas)
96
Why should PRP be reserved for small lesions at tendon/bone interfaces?
(Bc PRP can induce fibrosis in large lesions, its okay for small lesions to have some fibrosis)
97
Is IV or IA administration of certain regenerative therapies thought to have a better chance of getting to a tendon injury?
(IA)
98
Why should bone marrow stem cells not be used when tendons have calcification?
(Bc bone marrow stem cells can induce more calcification)
99
What location on the suspensory ligament is more commonly injured?
(Proximal suspensory, right at the origin)
100
Is hindlimb or forelimb suspensory ligament injury associated with a poorer prognosis?
(Hindlimb, and of course that is where it is more likely to occur in dressage horses)
101
What is the primary function of the suspensory apparatus?
(Support the MCP/MTP joint)
102
Which horse breeds are genetically predisposed to degenerative suspensory ligament desmitis aka equine systemic proteoglycan accumulation?
(Paso Fino horses, quarter horses, and warmbloods)
103
What conformations are risk factors for suspensory ligament injury?
(Straight hocks and dropped fetlocks)
104
What is the singular nerve that innervates the suspensory ligament?
(Deep branch of the lateral palmar/plantar nerve)
105
What are the goals of suspensory ligament desmoplasty and fasciotomy?
(Decompress acute lesions and promote new blood supply in chronic lesions)
106
Are hind or forelimbs most often affected by angular limb deformities?
(Forelimbs)
107
Of the sites where angular limb deformities occur (fetlock, tarsus, carpus), rank them from most to least common.
(Most common → carpus, fetlock, least common → tarsus)
108
What are perinatal factors that can lead to congenital angular limb deformities?
(Intrauterine malpositioning, overnutrition of the mare, cuboidal bone hypoplasia, and incomplete development of MT/MC II and IV)
109
What are the two ways that angular limb deformities can be acquired?
(Asynchronous longitudinal growth of the physis or traumatic luxation/fracture)
110
(T/F) Mild carpal valgus is thought to be protective against carpal injuries and therefore even mild carpal varus is bad.
(T)
111
For hoof extensions, would you use lateral or medial extensions to correct varus deformities?
(Lateral extension for varus, medial for valgus)
112
Is periosteal transection and elevation performed on the side of the limb that is growing too slow or too fast?
(Too slow, goal of PTE is growth acceleration)
113
If performing a PTE for treatment of a valgus deformity, will the PTE need to be performed medially or laterally?
(Lateral)
114
What is the goal of transphyseal bridging?
(Slowing growth on the convex side of an angular limb deformity)
115
If performing transphyseal bridging on a valgus deformity, will the TPB need to be performed medially or laterally?
(Medially)
116
If you are dealing with a MCP or MTP angular deformity, treatment should occur before what age to ensure there is enough growth to correct the deformity?
(30 days)
117
If you are dealing with a carpus or tarsus angular deformity, treatment should occur before what age to ensure there is enough growth to correct the deformity?
(4 months)
118
What are two causes for acquired tendon/ligament laxity?
(Hoof overgrowth or bandaging/casting for long periods of time)
119
What structure can be cut surgically to fix distal interphalangeal joint flexural deformities?
(Distal check ligament)
120
What structure can be cut surgically to fix metacarpophalangeal joint flexural deformities?
(Proximal check ligament)
121
Do you want a toe or heel extension for DIP flexural deformities?
(Toe extensions, and should trim the heel)
122
(T/F) Normal joint motion is pain-free, follows a prescribed range of motion, and is virtually frictionless.
(T)
123
(T/F) Normal joint motion is controlled by muscles and tendons and is repeatable.
(T)
124
In what two locations of the body are menisci used in joints?
(The stifle and the TMJ)
125
The term osteoarthritis is a term that represents a group of disorders that are characterized by what three things?
(Deterioration of articular cartilage, changes in the subchondral bone, and changes in soft tissue of joints)
126
(T/F) Natural repair processes of articular cartilage by adjacent tissues are incapable of producing tissue with morphological, biochemical and biomechanical properties of articular cartilage.
(T, cartilage defect → fibrous tissue → fibrocartilage (not the same as original cartilage))
127
The chondrocyte response to biomaterial failure as a result of trauma is to degrade a repair what they can but that results in what pathology?
(Chronic synovitis)
128
A joint will form enthesophytes and osteophytes to try to fuse a joint that is causing pain due to injury but that only works in high/low (choose) motion joints.
(Low)
129
What histopathologies occur in the synovial membrane in osteoarthritis?
(Synovial lining hyperplasia, villous hyperplasia, inflammatory cell infiltration of subintima, and fibrosis)
130
If a synovial insult or injury occurs, synoviocytes will release what substances?
(Lysosomal enzymes, PGE2, free radicals, and cytokines)
131
What are the sources of pain associated with synovial insults/injuries?
(There are pain receptors in the capsule itself so triggering of those leads to pain but also the increase in intraosseous pressure leads to pain)
132
Why is articular cartilage that is undergoing degradation discolored?
(Because of the loss of proteoglycan, instead of nice pale white it will start to turn yellow)
133
What types of strength that articular cartilage provides a joint are reduced when that cartilage is degraded?
(Compressive and tensile strength)
134
What is the main purpose of chondrocytes in the joint?
(Controlling the turnover over the extracellular matrix of articular cartilage)
135
The turnover of the extracellular matrix of articular cartilage by chondrocytes is controlled by what?
(The local environment so cytokines present and mechanical stimuli)
136
Pair the following cytokines to the metabolic pathway they trigger when present in the joint:
IGF and TGF
A - Anabolic
B - Catabolic
C - Regulation of catabolism
(A)
137
Pair the following cytokines to the metabolic pathway they trigger when present in the joint:
IL-1, TNF-a, IL-17 and prostaglandins
A - Anabolic
B - Catabolic
C - Regulation of catabolism
(B)
138
Pair the following cytokines to the metabolic pathway they trigger when present in the joint:
IL-10, IL-4, IL-6, IL-13
A - Anabolic
B - Catabolic
C - Regulation of catabolism
(C)
139
How does subchondral bone adapt to repetitive cyclic loading?
(By becoming thicker)
140
What subchondral bone changes are seen in relation to osteoarthritis?
(Subchondral bone sclerosis, subchondral cystic lesions (d/t vascular infiltration or focal osteonecrosis), and periarticular osteophyte formation)
141
What are the two essential clinical features of osteoarthritis that are the main reason it is treated?
(Pain and loss of function)
142
What are nonsteroidal anti-inflammatory options for treatment of inflammation secondary to trauma or degraded cartilage products in osteoarthritis?
(Phenylbutazone, flunixin meglumine, firocoxib, diclofenac sodium, acetaminophen)
143
What is the purpose of Adequan (an IM injectable polysulfated glycosaminoglycan)?
(Stimulates synoviocytes to produce hyaluronic acid, stimulates chondrocytes to produce proteoglycans and collagen, and inhibits metalloproteases)
144
Why is pain relief associated with corticosteroid intra-articular injections both an advantage and a disadvantage?
(Pain relief is an advantage but also a disadvantage because it can hides big issues like fractures)
145
How does intra-articular corticosteroid usage improve cartilage nutrition?
(By controlling severity of synovitis → enables return of normal synovial fluid properties and improves fluid exchange within the joint)
146
What is an important differential diagnosis for post-injection flare symptoms (heat, pain, swelling, and lameness that occurs 8-24 hours post-injection of corticosteroids)?
(Joint infection)
147
What is thought to enhance the positive effects of corticosteroid intra-articular injections so they are often combined (though this has not been studied)?
(Hyaluronic acid)
148
What is the primary adverse effect of IA polysulfated glycosaminoglycans that IA HAs do not have?
(Increased chance of infection → increased minimum inhibitory concentration of abx effective in vitro against S. aureus, don’t use with steroids)
149
What does IRAP stand for?
(Interleukin-1 receptor antagonist → competes with IL-1 for binding and IL-1 is one of the main actors for bad OA)
150
The primary goal of arthroscopic techniques for repairing cartilage is enhancement of what the body is already doing to repair the tissue either by increasing the quantity or quality of the repair tissue, how is that accomplished?
(Local manipulation or cell/tissue transplantation)
151
What are the advantages and disadvantages of a chondroplasty for partial thickness defects?
(Advantages → removal of loose tissue and reduction of further exfoliation which will prevent further synovitis, disadvantage → no long term improvement)
152
Is a partial or full thickness defect in articular cartilage going to induce an improved healing response?
(Full thickness, will trigger extrinsic repair which entails mesenchymal tissue inflow from subchondral bone, partial thickness defects only trigger an intrinsic repair)
153
What arthroscopic surgical technique can be utilized to aid extrinsic repair efforts?
(Making microfractures in the subchondral bone → better quality of fibrocartilage healing, increased type II collagen)
154
If you can make sure that your surgical approach to arthrodesis is very stable, it can decrease the time the horse needs to be in a cast, why is that a good thing?
(Less chance of secondary issues due to casting such as wounds/pressure sores and a shorter hospital stay)
155
Why is there only a mild to moderate increase in white cell count with post steroid injection infections?
(Bc steroids are blocking WBC normal action)
156
Foals are typically the culprit in hematogenous joint infections, what types of foals are going to get joint infections more likely?
(FPT foals and foals with a septic process (which likely are also FPT foals))
157
If you have a lame adult horse with a fever, are you jumping straight to the conclusion of a septic joint?
(No, if an adult horse with lameness/pain/swelling has a fever, it is more likely due to a cellulitis rather than a joint infection; fever is usually more associated with foals and septic joints)
158
If you have a septic foal that you have been monitoring twice daily for effusion and once daily for lameness that is now lame and has an effusive joint, what should you do?
(An arthrocentesis, submit for c/s)
159
When you have a wound that is over a joint and you want to tap the joint to discover if it has been compromised, where should you perform the tap and why?
(Away from the wound, do not want to track infection from wound to joint if there is not joint compromise; can then also distend the joint to see if it holds fluid or if it communicates with the wound)
160
What would you expect the serum amyloid A to be at least in a patient with a septic joint?
(>60 mg/L)
161
On an ultrasound of a septic joint, you would expect to see an increase/decrease (choose) in synovial fluid and an increase/decrease (choose) in echogenicity of synovial fluid.
(Both increase)
162
Finding gas in the synovial fluid on ultrasound of a septic joint may indicate what process?
(Anaerobic bacteria are forming gas)
163
Why is there a poorer prognosis associated with a joint infection of a joint with osteoarthritis?
(OA damage leaves a fibrous layer on affected cartilage which is easier for bacteria to colonize and hide in during tx)
164
If the WBC count of synovial fluid is 10,000/uL, what process is indicated?
(Inflammation, <450-5000 is normal, 5,000-20,000 is inflammation, >30,000 is infection)
165
If the total protein of synovial fluid is 4.2 g/dL, what process is indicated?
(Infection, <2.0 g/dL is normal, <2.5 g/dL is inflammation, and >4.0 g/dL is infection)
166
What value of neutrophils in the synovial fluid is pathognomonic for sepsis causing a joint infection?
(>95%)
167
(T/F) In acute cases of joint infections and with a healthy horse, broad spectrum antibiotics and a thorough lavage will resolve most infections.
(T)
168
What is primarily the issue when the tendon sheath is damaged in association with joint infections?
(Inflammatory mediators can cause adhesions > loss of normal motion)
169
What are the maximum doses of gentamicin and amikacin that can be used for systemic and intra-articular CRIs?
(Gentamicin 600mg/day, amikacin 2500mg/day)
170
What is the main prognostic indicator for septic tendon sheaths?
(Time, how long it took to start treatment, longer is worse prognosis; kinda the same for joints too)
171
What are the two types of muscle atrophy and which fiber types are they associated with?
(Myogenic atrophy, type 2 fibers; neurogenic atrophy, type 1 and 2 fibers)
172
What are two etiologies of muscle fasciculations?
(Abnormal recruitment of nerves (can occur in response to nerve root irritation, electrolyte abnormalities, weakness, fatigue, anxiety, and cold) or ion channel defects within the sarcolemma (HYPP))
173
What electrolyte excessively accumulates in muscle cells in relation to rhabdomyolysis that then triggers mitochondria to produce free radicals, proteases, phospholipases, and inflammatory cytokines?
(Calcium)
174
Is creatine kinase better for indicating acute/chronic (choose) injuries?
(Acute, peaks w/in 4-6 hours and returns to normal in 48 hours, severe >4000u/L increases associated with muscle damage)
175
How long does it take for aspartate aminotransferase to return to normal after insults to muscle, liver, RBCs, and other tissue AST is found in?
(Weeks, peaks in 24 hours post injury)
176
What value of serum CK will indicate a positive test in a serum CK exercise response test?
(>3x increase in CK from baseline)
177
What electrolyte changes do you expect to see in severe rhabdomyolysis cases?
(Hyponatremia, hypochloremia, hypocalcemia and hyperkalemia, hyperphosphatemia)
178
Why should you monitor the kidney values in horses with muscle disease?
(Bc myoglobinuria is associated with renal tubular necrosis)
179
What substance should be tested for in foals with severe rhabdomyolysis?
(Selenium)
180
What vitamin should be tested for in horses with generalized muscle atrophy?
(Vitamin E)
181
Of the clinical signs associated with muscle disease in horses, which is not associated with changes on muscle biopsy?
(Muscle fasciculations)
182
Pair the muscle disease with the muscle(s) that should be sampled:
Exertional rhabdomyolysis, PSSM
A - Sacrocaudalis dorsalis
B - Semimembranosus, middle gluteal
C - Gluteal or lumbar
(B)
183
Pair the muscle disease with the muscle(s) that should be sampled:
Immune-mediated myositis
A - Sacrocaudalis dorsalis
B - Semimembranosus, middle gluteal
C - Gluteal or lumbar
(C)
184
Pair the muscle disease with the muscle(s) that should be sampled:
Generalized muscle atrophy
A - Sacrocaudalis dorsalis
B - Semimembranosus, middle gluteal
C - Gluteal or lumbar
(A)
185
What veterinarian should you look up when you’re sending in a muscle biopsy because she’s the best?
(Dr. Stephanie Valberg)
186
What is the main preventative strategy for PSSM episodes?
What is the main preventative strategy for PSSM episodes? (Decrease starch in diet/no grain and daily exercise)
