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Moving Exam 1 GO LOOK AT THE OTHER ONE > LA Orthopedics > Flashcards

LA Orthopedics Flashcards

1
Q

What is the exercise-response test?

A

Measure serum CK before and after 4-6 hours after modest exercise (15 minutes of trotting)

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2
Q

What is a normal reading of the exercise-response test?

A

less than 3-4 fold increase in CK

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3
Q

What is Polysaccharide storage myopathy?

A

genetic disorder that causes glycogen storage disorders

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4
Q

What is Type 1 PSSM?

A

Genetic mutation that causes glycogen accumulation inside the cells and formation of abnormal polysaccharide

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5
Q

What is Type 2 PSSM?

A

Unknown cause that upon muscle biopsy shows clumping of muscle glycogen but do not have type 1 PSSM

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6
Q

What are the clinical signs of PSSM?

A

Muscle stiffness
Reluctant to move, exercise
Exercise intolerance
Overt muscle contractions
History of ER/poor performance

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7
Q

How would you treat acute muscle disease in PSSM?

A

Stall rest then pasture out
Relieve anxiety (Acepromazine)
Restore fluids and acid/base balance with IV fludis
IV DMSO
NSAID—NEPHROTOXIC
FC water
Hay only no grain

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8
Q

How to prevent PSSM muscle disease?

A

Standard daily routine
Minimize stress
Daily exercise
Long slow warm up periods
Balanced diet

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9
Q

What are the characteristics of a balanced diet to prevent PSSM muscle disease?

A

manage caloric intake
Avoid lush pasture high in sugars
High quality grass hay
Electrolyte supplemet with first ingredient is salt

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10
Q

What is the cause of post-anesthetic myopathy?

A

hypoperfusion

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11
Q

How can you prevent post-anesthetic myopathy?

A

maintain blood pressure & good oxygenation and minimize down time

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12
Q

What is Hyperkalemic Periodic Paralysis?

A

Genetic disorder in which there are defective voltage-gaited sodium channels allowing sodium to leak in to cells causing resting potential to be close or overlap with threshold resulting in hyper excitability

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13
Q

What are the main clinical signs or history involved with HYPP?

A

Caused by a “trigger”
Prolapse of the third eyelid
Recumbency. dog sitting

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14
Q

What are the “triggers” for HYPP?

A

Ingestion of high potassium diet
Sudden dietary changes
Fasting
Anesthesia
Heavy sedation
Trailer rides
Stress

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15
Q

How do you diagnose HYPP?

A

History of “impressive” breeding
Characteristic clinical signs
Hyperkalemia
**DNA analysis*****

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16
Q

What is the emergency treatment for HYPP?

A

IV calcium gluconate or IV dextrose
Tracheostomy

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17
Q

What is the treatment for mild HYPP episodes?

A

Stall rest
Hand walking
Grain meal or corn syrup orally
IM Epinephrine
Acetazolamide
Observation for worsening

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18
Q

What is the prognosis of Rhabdomyolysis?

A

Good to guarded depends on managment

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19
Q

What is the prognosis of PSSM?

A

Good with proper management

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20
Q

What is the prognosis of HYPP?

A

Good in most cases
Severe cases may be fatal
DO NOT BREED affected animals
Advise before sedation/anesthesia

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21
Q

What are the types of information that should be collected when you are taking a history from an owner with a lame horse?

A

Signalment (breed & age)
Acute vs. insidious onset (duration)
Use of the animal
Managments (shoeing intervals & exercise routines)

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22
Q

What are the grades of the AAEP lameness scale?

A

Grades 1 through 5

23
Q

What does grade 1 mean on the AAEP lameness scale?

A

Difficult to observe, inconsistent

24
Q

What does grade 2 mean on the AAEP lameness scale?

A

Difficult to observe at walk/trot going straight; consistent in circle, incline, hard surface

25
Q

What does grade 3 mean on the AAEP lameness scale?

A

Consistently observable at trot

26
Q

What does grade 4 mean on the AAEP lameness scale?

A

Obvious at walk; marked nodding/hitching/short stride

27
Q

What does grade 5 mean on the AAEP lameness scale?

A

Minimal weight bearing, inability to move

28
Q

What are the cues that help determine which forelimb are lame in a horse?

A

Head bob- down on the sound
Arc of flight of foot
Altered flight path of foot
Length of stride
Angles of joint flexion
Audible differences between limbs

29
Q

What are the cues that help determine which hind limb are lame in a horse?

A

Pelvic hike or drop- up/down on the lame limb
Arc of flight of foot
Altered flight path of foot
Length of stride
Angles of joint flexion
Drifting away from lame limb

30
Q

What is the proper order of procedures during a lameness examination?

A

History
Thorough physical exam
Baseline motion exam- establish lameness grade
Manipulations- hoof testers, flexions, diagnostic analgesia
Diagnostic imaging

31
Q

How does action of the reciprocal apparatus affect performance of a lameness examination, including flexion tests?

A

The reciprocal apparatus flexes everything so if we were to pick up the hind leg, all of the joints automatically flex to some degree

This makes it difficult to perform flexion tests

32
Q

What structures are stressed during performance of digit flexion tests? Are these tests sensitive and specific?

A

Distal interphalangeal joint (Coffin joint)
Proximal interphalangeal joint (Pasturn joint)
Metacarpophalangeal joint (Fetlock joint): passively flexed, not putting a lot of pressure on it

Nonspecific and nonsensitive

33
Q

What structures are stressed during performance of carpal flexion tests? Are these tests sensitive and specific?

A

Metacarpophalangeal joint (Fetlock joint)

Nonspecific and nonsensitive

34
Q

What structures are stressed during performance of hind limb flexion tests? Are these tests sensitive and specific?

A

The whole leg is flexed to some degree due to the reciprocal apparatus

Pressure would mainly be on the distal interphalangeal joint if that is the joint to be examined

Nonspecific and nonsensitive

35
Q

What structures are stressed during performance of a Hock/stifle manipulation test ? Are these tests sensitive and specific?

A

Pressure would mainly be on the hock/stifle joint if that was to be examined as well

Again not a lot of pressure on the rest of the leg

Nonspecific and nonsensitive

36
Q

How does the order of the lameness examination differ for horses with severe (grade 4/5 or 5/5) lameness?

A

Start with Radiographs first
Then move to block out the lameness

37
Q

What structures are desensitized by palmar/plantar perineural blocks?

A
  • Sole
  • Digital cushion
  • Navicular bone
  • Navicular bursa
  • Navicular suspensory apparatus
  • Insertion of deep digital flexor tendon on P3
38
Q

What structures are desensitized by Abaxial sesamoid perineural blocks?

A
  • Mid-body/base of the proximal sesamoid bones
  • Dorsal hoof wall
  • Coronary band
  • Coffin joint
  • Pastern joint
  • Sesamoidean ligaments
39
Q

What structures are desensitized by Low 4-point perineural blocks?

A
  • Fetlock joint
  • Sesamoid bones
  • Insertion of suspensory ligament on the sesamoid bones
40
Q

What structures are desensitized by high 4-point perineural blocks?

A
  • Fetlock joint
  • Sesamoid bones
  • Canon bone
  • Splint bones
  • Suspensory ligament
41
Q

What structures are desensitized by Wheat perineural blocks?

A

Intended to block the suspensory ligament

42
Q

What local anesthetics are commonly used in horses? Which is the most commonly used for diagnostic analgesia, and why?

A

Lidocain
Mepivacaine
Bupivacain

Mepivacaine is used more commonly because of the rapid onset with a longer duration

43
Q

What are the risk factors for steroid induced laminitis, and how common is it?

A

Triamcinolone use; it is not very common but we need to be aware of it.

44
Q

What are the most important cytokines involved in arthritis? What are their natural inhibitors?

A

Interleukin-1
Prostaglandin E2

45
Q

What are the most important degradative enzymes involved in arthritis? What are their natural inhibitors?

A

Matrix metalloproteinases
» MMP-1 – collagen
» MMP-3 – proteoglycan, cleaved collagen
» MMP-13 – collagen; faster than MMP-1

Aggrecanase

46
Q

What are the likely mechanisms of the initiation of arthritis?

A

Mechanism 1 – defective cartilage/bone with abnormal biomechanical properties
Mechanism 2 – abnormal change in subchondral bone
Mechanism 3 – normal cartilage exposed to abnormal forces
Combination of all three may cause Osteoarthritis (OA)

47
Q

How does exercise affect subchondral bone in horses, and how is that related to development of arthritis?

A

High intensity exercise leads to SCB sclerosis leads to Microdamage leads to Ischemia which leads to Necrosis which leads to Osteochondral collapse

48
Q

why may we not see coffin bone fractures radiographically and when should imaging should be repeated?

A

Due to the lysis along the fracture line, the fracture may not show up for 10-14 days, repeat at that point.

49
Q

What are the treatments for coffin bone fracture types?

A

» Types I, II, II, V – immobilize hoof wall (shoeing, cast, call surgeon?)
» Types II, III, IV – lag screw, difficult
» Types IV – surgical (removal, lag screw)

50
Q

What are the prognosis for P3 fractures?

A

» Types I, II – good
» Types III, IV – guarded-fair
» Type V – good (trauma), guarded (osteomyelitis)
» Type VI – excellent
» Depends on extent of articular involvement, presence of sepsis
» May need to do PD neurectomy after complete healing

51
Q

What are the common configuration, treatment, and prognoses for P2 fractures?

A

Etiology – sudden stops and turns on supported leg
Diagnosis – PE, radiographs, sudden acute lameness

Prognosis –
▪ Arthrodesis of PIP joint – good
▪ Involvement of DIP joint – guarded
▪ Conservative management – poor

52
Q

What are the common configuration, treatment, and prognoses for P1 fractures?

A

» Configuration – usually sagittal plane, initiate at fetlock joint
» Etiology – high speed injury
» Diagnosis – PE, presence of comminution/ displacement/ incomplete vs complete, acute lameness
» Treatment – no intact strut of bone, internal fixation alone (poor prognosis), transfixation cast or external fixator
» Prognosis (with surgery)
▪ Excellent for non-comminuted, incomplete, non-displaced, complete fxr that exits lateral cortex
▪ Fair/guarded – pastern joint involvement
▪ Poor – no intact strut

53
Q

What are the common configuration, treatment, and prognoses for MC3 condylar fractures?

A

» Configuration
▪ Lateral condyle – sagittal plane, incomplete, complete/non-displaced,
complete/ displaced
▪ Medial condyle – short, spiral, Y-fracture
» Etiology – high speed injury, remodeled bone, lateral condyle of forelimb most common
» Diagnosis – acute severe lameness, TAKE RADS FIRST
» Treatment – incomplete or non-displaced condylar fracture – conservative care, surgery necessary for some condylar fractures
» Prognosis (incomplete condylar fracture) – good prognosis for pasture soundness, delayed healing at articular surface

54
Q

What is the differential diagnoses for a ‘dropped elbow’ stance.

A

suprascapular nerve injury (harness collar, acute trauma)

» Acute lateral scapulohumeral instability
» Delayed atrophy of supraspinatus, infraspinatus (2-8 weeks)
» Treatment – exercise restriction, NSAIDS, cold hydrotherapy, topical anti
inflammatories, surgical decompression
» Prognosis – good for function, muscle atrophy may remain

Moving Exam 1 GO LOOK AT THE OTHER ONE (8 decks)

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