Week 3 27/5/14 LOCOMOTION (WEEK 1) Flashcards

1
Q

The head sinks when weight is on the ___limb

A

Head sinks ‘nodding’ when weight is on sound limb e.g. the lameness is on the contralateral limb Head raises on affected limb

Drop on the sound!

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2
Q

Signs of hindlimb lameness in dogs (2 things)

A

CHECK ANSWER!!!!!!!

??????!!!!!!!!

Think hip dips on lame leg BUT raises in horses?????

Hock drops more on __ side???

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3
Q

In horses, which gait is not useful for detecting subtle lameness

A

The walk is NOT useful for detecting subtle lameness.

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4
Q

What is pelvic hike?

A

Pelvic limb lameness in horses. Pelvic hike (raise of the pelvis) when affected limb is weight bearing When sound limb is weight bearing there is a drop of pelvis

c.f. DOG= DROP OF PELVIS WHEN AFFECTED LIMB BEARS WEIGHT

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5
Q

What is drifting?

A

Horse moves away fro affected limb (underbody placement of the affected limb)

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6
Q

How does increasing in speed increase the force?

A

Increase in speed–> shorted stance –> higher force

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7
Q

What type of forces do a) bones b) tendon?

A

a) Bones: Tension, Compression, Bending b) Tendon: Tension

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8
Q

Which are the two high stress structures in the equine distal limb?

A

SDFT and SL (suspensory ligament) ‘S’tress more ‘S’uperficial

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9
Q

What are the low strain structures?

A

DDFT and DAL (Accessory ligament)

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10
Q

What is the SDFT injured more than the suspensory ligament?

A

SDFT and SL are both high stress tendons and have SIMILAR FORCE but the SDFT has a HIGHER STRESS

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11
Q

How does the change in surface compliance affect horses DIFFERENTLY from humans?

A

Humans: have muscles therefore can change ‘stiffness’ Horses: No muscles therefore can’t alter ‘stiffness’ of muscles therefore can’t adjust to different surface compliances

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12
Q

The type of muscles in flexor tendon muscles

A

Flexor tendon muscles are highly pennate with 1cm muscle fibres. Limited capacity for length change

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13
Q

What is the slip and glip mechanism a) on soft surface b) turf

A

The hoof lands on a soft surface then slides along to reduce impact (soft surface). On turf there is less sliding and therefore more impact on the hoof

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14
Q

What are the protective mechanisms of the hoof?

A

-Shape of solar surface -Suspension of distal phalanx: forces transferred via distal border of hoof wall -Digital cushion -Hoof sliding -Rotation/ Translation of the DIP joint

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15
Q

What is the duty factor (related to locomotion)

A

The duty factor is the RATIO of the stance and stride time. e.g. higher forces when trotting as shorter stride length (and duty factor)

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16
Q

During the gallop, the front limb of the horse experiences forces of up to ____ x body weight

A

Walk: 1/2 times body weight Gallop: 2.5 times body weight 1

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17
Q

Aetiological theories for sole ulcers in cows

A

Loss of laminar suspension around calving Loss of dat bad Long standing times Laminitis and drop/ rotation of PIII

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18
Q

Aetiological theories for white line disease

A

Little evidence published. - Biotin deficiency - Loss of fat pad - Soft claws during high rainfall (NZ cows) - Over trimming - Sharp turns on concrete - Rough, stoney tracks

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19
Q

Aetiological theories for Digital dermatitis

A

Three families of treponeme, gaining entry through hair follicles. Sequalae: Interdigital hyperplasia

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20
Q

Which bacterium causes foul foot?

A

Fusobacterium necrophorum Sequlae: Interdigital hyperplasia

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21
Q

Aetiological theories of toe necrosis

A

Treponemes invading from coronary band in interdigital space. Entry through over- trimmed toes

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22
Q

What is Laminitis

A

Laminitis is characterised by failure of the attachment of the epidermal cells of the epidermal (insensitive) laminae to the underlying basement membrane of the dermal (sensitive) laminae

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23
Q

Risk factors for Laminitis

A

Associated with -Sepsis/ Systemic inflammation (GI disease, pneumonia, septic metritis), endocrine disease (PPID/EMS), mechanical overload or access to pasture

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24
Q

Pathogenesis of Laminitis

A

Developmental –> Acute Laminitis –> Resolution or progression to Chronic Laminitis (depending on effectiveness of treatment)

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25
How long is the developmental stage in the pathogenesis of laminitis
Developmental stage is the contact with the trigger and lasts around 72 hours. It is impossible to determine when a horse is in the development stage of laminitis
26
In dogs, head raises when weight is placed on the
Affected limb. Head drops when weight in placed on sound limb i.e. affected in contralateral
27
How do lameness scales vary in dogs and horses
Dogs: 1-10 (if you can see it must be \>grade 2) Horses 1-5
28
In horses the pelvis drops when the ___ limb is weight bearing
Pelvis drop occurs when sound limb weight bearing Pelvis hike occurs when lame limb is weight bearing.
29
Which tissues undergo tension
Tendon and bones
30
Dystrophic calcification
Necrotic/ damaged tissue calcification. = calcinosis circumscripta.
31
Which DAMNITT is very unusal in bone
Autoimmune very uncommon Degenerative: more related to joints Inflamm: more related to joints
32
Osteromyelitis is
infection of the cortical bone and medullary cavity . Osteitis is inflamm of the cortex without the involvement of the red/yellow bone marrow
33
2 most used Bone antibiotics
1. Clindamycin 2. Tetracyclines.
34
Treatment of Osteomyelitis
Early intervention with broad spec antibiotics (clindamycin/tetracycline). Change on basis of culture Consider local selivery
35
Radiographic changes associated with osteomyelitis and osterosarcoma (similar)
Combination of lysis and bone formation
36
10 yr old greyhound, unilat forelimb lameness 3 week duration. Non responsive to analgesia/ restriction in exercise. Pain on deep palpation of distal radius. Swelling at distal radius. Likely diag
Lateral radiograph showed lysis, loss of cortical density and aggressive perisoteal bone formation. Bone biopsy = osteosarcoma. ANALGESIA WILL NOT BE SUFFICIENT= UNREMMITING
37
Prognosis of osteosarcoma
Discuss with owner as NEARLY ALL osteosarc have micro mets in lungs at time of diagnosis (might not be visible) Osteosarcs can be lameness to life ending in 3 weeks.
38
Osteosarcoma treatment
Amputation (4 months) Amputation and Chemo (12 months) NSAIDs/Bisphosphates (palliative) Radiotherapy (palliative only)
39
How does massage work
Relaxation (lowered stress) Pain relief via lowered stress and possible endorphine release Direct activation of neuropeptide release Improved circulation and lymphatic flow (and return)
40
Difference between stroking and Effleurage
Stroking: Proximal to Distal Effleurage: Medium pressure Distal to Proximal
41
Compression and Wringing is known as How long to compress muscles for
Petrissage. Higher pressure at individual muscles. Compress and hold for 15 minutes
42
How long should Cryotherapy be used for
20 minutes. Affects vasculature (constriction) and nerves (analgesia) directly. Can be used when patient is NOT AMBULATORY i.e. can be used in ACUTE PHASE
43
Thermotherapy cannot be used when?
Thermotherapy cannot be used in the ACUTE phase. Also affects vasculature (constriction) and nerves (analgesia). If used in acute phase will make swelling, heat and pain worse. Helps vasodilation
44
Thermotherapy is contraindicated
IN ACUTE PHASE. WILL MAKE SWELLING ETC WORSE. Use Cryotherapy
45
Passive Range of Motion vs Active Assited ROM
Passive ROM can be used before patient wants to stand (analgesia?) Active Assisted ROM used once patient starts to walk.
46
Passive ROM number of repetitions
Can be used before patient wants to stand (analgesia?) 15-20 repetitions, 2-4 times daily.
47
Active ROM
Patients that are walking/trotting normally do not use full ROM. Change exercise to encourage use of full ROM.
48
Stretching =
Taking joint past normal ROM. Designed to opposite shortening of tissues and to break down fibrosis and adhesions. Hold for 15 seconds and gently release. Up to 20 x per session
49
How does Ultrasound work in rehab?
Primarily works through a heating effect and has the capacity to heat deeper tissues (microwave!) Short treatments (10 minutes) Tendinits, Bursitis, Joint contracture
50
Electrical stimulation
Neuromuscular electrical stimulation. Increases muscle mass, strength and oxidative capacity. May have analgesic effect.
51
Difference in hertiability values in Elbow dysplasia and Hip dysplasia
ED: 50-70% HD: 20-30% (still v. high) Polygenic disease
52
Pathogenesis of Hip dysplasia
Ligament hypertrophy -slack ligaments Subluxation - ball and socket not together Destruction of cartilage Change of shape of joint surface LEADS TO SECONDARY OSTEOARTHRITIS Both primary changes and secondary changes can be picked up by radiograph.
53
Which two ligaments are primariliy effected by hip dysplasia
Capsular ligament and Teres ligament. Subluxation - cartilage surfaces still in contact)
54
Where would you find the capsular ligament and the Teres ligament
Capsular most important
55
In a dog with HD when would pain be expected
Hip ROM normal. Bilateral pain at full extention.
56
Why do dogs with HD have a circumducting gait
Circumduction legs to keep pelvis flat and avoid subluxating. Lux via Sublux (cartialge still in contact)
57
Which ligament is most involved in pathogenesis of hip dysplasia
58
If angle and luxation and angle of subluxation are close then \_\_\_\_\_\_\_
Shallow acetabulem
59
How do signs of HD differ at a) 0-6 months b) 6-16 months c) \> 16 months
a) 0-6 months: Subluxation / Abnormal gait b) 6-16 months: Sublux/Abnormal gait. Sublux/ Damage & Damage/ Inflamm/ Pain, Lameness c) Muscular fibrosis/ fibrosus stabilisation. Painfree restricted range
60
Can Hip Dysplasia by non painful?
Yes. 0-6 months: abnormal gait due to sublux 16 months on Abnormal joint, secondary OA, Pain, Lameness OR Pain free / restricted range due to Muscular/fibrosis stabilisation
61
When does restricted range develop in HD?
16 months on due to muscular/fibrosis stabilisation. Pain free restricted range.
62
What is the Ortolani test?
Ortolani test: do Barlow sign then abduct the limb to see if there is a palpable clunk noted as the femoral head reduces into the acetabulum. Most young dogs have some hip laxity so the accuracy of palpation is poor in puppies at 6-18 weeks of age but improves as dogs approach 6 months old. ORTOLANI: TRY TO REPLACE BARLOW: TRY TO DISPLACE
63
Treatment of Hip Dysplasia a) 0-6months b) 6-16 months c) 16 months +
0-6 months: Conservaitve Diet/Exercise 6-16 months: Conservative Diet/Exervise Surfical correction Anat. correction\* 16months+ Conservative / Hip replacement/ Ex Arthroplasty \* OVER 15-20 KG
64
Conservative treatment for Hip Dysplasia
Exercise control NOT restriction.
65
When can surgical treatment of hip dysplasia be considered
hip replacement at 16 months Dogs over 15-20kg
66
Cartilage properties
Collagen Proteoglycans Water Resident cells: Chrondrocytes responsible for turnover Hyaline cartilage provides interface btween bones at synovial joint
67
Damage to the Metaphysis/Physis/Epiphysis can cause shortening/ deformity
Damage to the Physis (only present in Juvenile) can cause temporarly or permenant arrest
68
Osteochondrosis
Term for group of conditions of developing cartilage and supporting bone. e..g Osteochondritis dissecans (OCD) Osteochrondrosis is initiated by a vascular problem in the epiphysis. Failure of the normal cartilage to bone succession
69
Osteochrondritis dissecans (OCD) pathogenesis
Detachment of a chondral or osteochondral fragment from the articular surface Osteochondrosis (group of conditions of developing cartilage + supporting bone) initiated by a cascular problem in the epiphysis. Normal growth bone suceeds cartilage growth normally
70
3 examples of Osteochondrosis'
1 Osteochrondritis Dissecans 2. Subchondral bone cysts (SBC) 3. Peri-articular fragmentation/fracture e. g.medical coronoid fragmentation
71
Which species get subchondral bone cysts
Horses (also get Osteochondritis dissicans) Fast growing high performance patient
72
Which species get OCD
Osteochondritis dessicans. Initiated by a vascular problem in the epiphysis. Failure of the normal cartilage to bone succession. Dogs/ Horses (SBC)/ Pigs (esp hip) Broiler chickens (stifle)
73
Where does Osteochondritis dessicans occur in pigs vs chickens
Chickens: OCD stifle Pigs: OCD hip
74
Presentation of osteochondrosis
Young, fast growing large pure bred. Joint effusion Often bilat Variable lameness.
75
Surgical treatment of Osteochondrosis
Symtomatic/ Conservative/ Surgical open or arthroscopy (gracment removal. Prognosis guarded specific to joint
76
Primary disease in Canine Elbow Dysplasia
Osteochonrosis. ED includes: Humeral Osteochondritis dissecans Fragmented Cornoid process Ununited anconeal process Secondary osteoarthritis.
77
Main classification of canine arthritis
Non-inflammatory and Inflammatory (\>3000WBCS) Non-Inflamm further divided into traumatic, hemarthrosis, DJD
78
Inflammatory canine arthritis is further divided to
Infectious (bacterial, fungal, viral, rickettsial, protozoal) Non-infectious- Immune based (erosive- rheumatoid) Non-erosive )Idiopathic, polyarthritis) Non immune based- neoplastic/ crysyal
79
Hemathrosis
Bleeding into joint space (form of non inflamm (WBC \<3000) arthritis
80
Type of arthrocentesis for suspected polyarthritis (much more common than Rhumatoid arthritis)
Sample multiple joints as POLYarthritis
81
WBC from arthrocentesis from non-inflammatory arthritis e.g. DJD
\<3000 and few neutrophils (\<20%)
82
Macrophages in the synovial sample are indicitive of
Non-inflammatory. Also synoviocytes are normal for both samples
83
Inflammatory joint disease. Synoviocytes= normal
84
Degenerate joint disease. Non-inflamm Macrophages
85
What happens to the synvovial fluid: blood concentration in septic arthritis
Synovial fluid to blood ratio is normally 0.8-1 In septic arthritis it DECREASES.
86
TP in synovial fluid is normally \<
TP in synovial fluid is normally \<1g/dL Increased in inflammatory arthritis
87
Why should care be taken when culturing synovial fluid
23% negative in spite of infection (false negative) Careful with false positives. To improve use culture medium / synovial membrane biopsy
88
Most common cause of infection arthritis
Bacteria Direct penetration, spread from adjacent tissues/ Haemtogeneous. Staphylococcus, Streptococcus, Pastuerlla
89
How can radiology help you differentiate acute and chronic
Acute: Effusion Chronic: Degenerative Changes
90
Infectious arthritis when suspecting immune-mediated polyarthritis. Serology tests for...
1. Borrelial arthritis (Lyme disease) 2. Rickettsial arthritis (Tick not endemic to uk) 3/ Protozoal arthritis (Leishmaniasis) - tick not endemic to UK TRAVEL HISTORY!
91
Diagnosis of Rheumatoid arthritis
Rheymatoid factor. Antibodies against IgG. High titres in IgG. Radiographic changes
92
When suspecting immune-mediated polyarthritis. Which tests are appropriate
ANA titers: Anti-nuclear antibodies, High titres is Systemic Lupus Erythematosis (SLE) Other inflamm/infectious processes can lead to low titres SLE: Skin lesion, glomerulonephritis, haemolytic anaemia, polymyositis
93
Dog with skin lesions and arthritis affecting more than one limb- most likely Ddx
Systemic Lupus erythematosus (SLE) Appropriate test for polyarthritis is the ANA test. Also with SLE: Glomerulnephitis, haemolytic anaemia, polymyositis, leukopenia, thrombocytopenia
94
4 subtypes for immune-mediated polyarthritis
Type 1: Idiopathic (50%) Type 2: Infection (25 %) Type 3: GI gz Type 4: Neoplasia
95
How does Polyarthritis differ in the greyhound from other dog breeds
Polyarthritis is normally non-erosive but in the Greyhound is erosive Other erosive: Rheumatoid arthritis. PA of feline
96
Downwards rotation of pedal bone. Clear gas line. = laminitis
97
Hypertrophic pulmonary osteopathy
periosteal new bone growth occurs on the distal limb bones in association with a chronic, usually intrathoracic, inflammatory or neoplastic lesion. Pathogenesis is unknown, but theories include reflex vasomotor changes mediated by vagus increasing blood flow to extremities HEART WORM??
98
If the primary pulmonary hypertrophic osteopathy lesion is removed will the periosteal bone growth regress?
The lesions may regress
99