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239 Cards in this Set
- Front
- Back
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what connective structure binds the lateral and medial claws in the bovine?
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cruciate ligament
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what are the four components of the bovine solar surface?
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1. wall
2. white line (connects the sole with the wall) 3. sole horn 4. heel horn |
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in the normal bovine
- which limbs bear the most weight? - which aspect of the claw is larger? - how does pressure influence hoof growth? |
- front limbs bear the most weight
- lateral claw (especially of the rear limbs) are larger because of conformation - hoof grows in response to pressure |
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what are the two most common areas of lameness in cattle?
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1. foot (90%)
2. upper leg lameness (10%) |
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where do most lamenesses occur in cattle?
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the rear foot
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which aspect of the feet are most affected in lameness in cattle?
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- lateral claw in rear limbs
- medial claw in front limbs |
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what is the pathogenesis of laminitis in the bovine?
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- disturbance of the micro-circulation of the corium
- leads to breakdown of epidermal-dermal bond between the hoof and the pedal bone - pedal bone may become displaced |
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what is the major predisposing factor for lameness in the bovine?
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grain overload
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why does grain overload cause laminitis in cattle?
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- rumen acidosis results in release of vasoactive substances and metalloproteinases
- this results in edema, hemorrhage and necrosis of the corium and associated tissues - edema → tissue damage → imperfect horn and sole |
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what are five causes for laminitis in the bovine?
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1. grain overload (most common)
2. standing on hard surfaces 3. stand on feet for long time (e.g. if they are in pain from disease) 4. over-trimming 5. endotoxemia |
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why would metritis, mastitis, or pneumonia lead to laminitis in the bovine?
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because they are in pain and reluctant to lay down; standing for too long will cause laminitis
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what are four clinical signs of acute laminitis in cattle?
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1. walking gingerly (as if on egg shells)
2. arched back stance and gait 3. hesitant to walk 4. laying around more than usual |
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what are three important ways to prevent laminitis in cattle?
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1. proper dietary management to prevent rumen acidosis
2. limit time on hard surfaces 3. maintain adequate loafing areas |
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what is the technical term for sole ulcers in cattle?
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focal septic pododermatitis
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in cattle, a circumscribed loss of the horny sole resulting in exposure of the corium is called what?
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sole ulcers / focal septic pododermatitis
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what is the definition of focal septic pododermatitis in cattle?
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a circumscribed loss of the horny sole resulting in exposure of the corium
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what are five reasons why lameness in cattle is important?
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1. ↓ feed intake
2. ↓ reproductive efficiency 3. ↑ trauma 4. ↑ culling 5. animal welfare |
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what is a typical posture of a bovine that has hind limb lameness?
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"cow hock look"; bilateral valgus of the hock
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how long does it take to see solar hemorrhages in a cow with laminitis?
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2 months
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why do abscess form in the sole of the foot in cows with laminitis?
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because the hoof wall is weaker and this disrupts the integrity of the new horn that forms (i.e., the horn is imperfect)
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what drug can be used to treat acute laminitis?
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NSAIDs (e.g. ketofen, aspirin)
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what is the pathogenesis of a sole ulcer in the cow?
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- subacute laminitis
- excessive horn growth, pedal bone displacement, and a softer sole - excessive weight bearing and breakdown of the imperfect sole, exposing the corium |
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when are dairy cows most predisposed to sole ulcers? Why?
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- during the first 3 months of lactation
- she drops 1 BCS, which is nutritionally demanding, and also loses some of the fat pad in the foot |
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what is the proper treatment for a sole abscess in a cow?
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- debride and clean
- but a hoof block on the healthy claw to elevate the ulcer - do not bandage |
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when are antibiotics indicated in cows with a sole ulcer?
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when there is swelling of soft tissue (above the coronary band)
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what are two ways to prevent sole ulcers in cows?
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1. feed enough forage to prevent subacute laminitis
2. regular foot trimming to keep normal weight bearing |
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what is the layman's term for white line disease?
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gravels
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what is the pathogenesis of white line disease and sole abscess in the cow?
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- damage between white line and corium allows for defects
- sole horn reduced by damaged corium is softer than normal and more susceptible to penetration - bacteria enter defects and inflammatory response produces abscesses |
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how do you treat a sole abscess in the cow?
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1. drain the abscess
2. debride necrotic material 3. clean it out 4. pack with iodine and cotton 5. if swelling, give antibiotics 6. put a foot pad on the healthy claw |
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what are four other names for papillomatous digital dermatitis in the bovine?
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1. digital dermatitis
2. strawberry heel warts 3. hairy heel warts 4. Mortellaro's disease |
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what causes strawberry heel warts?
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Treponema spp. and other anaerobes
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what is the pathogenesis of strawberry heel warts?
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- skin exposed to organic material containing organisms
- skin damage due to environmental conditions - manure (ammonia), rough surfaces |
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what are some risk factors for cattle developing strawberry heel warts?
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- dairy cows > beef
- open herds, outside trimmers - environment |
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what is the treatment for strawberry heel warts?
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1. TOPICAL antibiotics (oxytet, LS)
2. BANDAGE - to maintain antibiotic 3. can spray 4. foot baths (oxytet or formalin) |
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what are four ways to prevent strawberry heel warts?
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1. improve hygiene
2. dry, comfortable bedding 3. reduce stocking density 4. vaccination (Serpens spp.) |
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what are two other names for interdigital phlegmon in cattle?
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1. necrobacillosis
2. foot rot |
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what is the main agent that causes bovine foot rot?
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Fusobacterium necrophorum
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what is the best way to diagnose foot rot?
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the smell
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how is bovine root rot treated?
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- floss the toes with bailing twine
- antibiotics (penicillin, oxytet, Ceftiofur - no withdrawal time) |
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what are two other names for interdigital hyperplasia in the bovine?
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1. Fibroma
2. corns |
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in the bovine, what are corns?
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proliferative growth between the toes
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what is the pathogenesis of corns in the bovine?
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- thickening of the interdigital skin of the lateral claw
- proliferation due to irritation - poor hygiene, claw conformation, and abnormal splaying of the toes - sole overgrowth |
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when is treatment of corns in the bovine indicated?
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if the animal is lame
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how are corns in the bovine treated?
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- surgery: dissect out the tissue from the interdigital space (aggressively, or it will grow back)
- wire the toes together so the tissues will not dehisce |
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what is the best way to prevent corns in the bovine?
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hoof trimming
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what are five common reasons for a downer cow?
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1. hypocalcemia
2. hypomagnesemia 3. spinal compression 4. calving paralysis 5. compartmental syndrome |
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what are four injuries that may cause calving paralysis?
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1. pelvic swelling (trauma during parturition pushes on nerves)
2. obturator paralysis → coxofemoral luxation 3. sciatic nerve damage 4. peroneal and tibial nerve damage (from recumbency) |
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which nerves are most susceptible to damage when a cow has been in lateral recumbency for too long?
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peroneal and tibial
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what are three causes of compartmental syndrome in cattle?
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1. trauma
2. excessive pressure during labor 3. compression from being down |
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what is the pathogenesis of compartmental syndrome?
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1. decreased perfusion leads to ischemia
2. ischemia causes membrane to dysfunction, allowing for calcium accumulation 3. muscle necrosis, edema, swelling, and compression within fascial sheath |
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what are three clinical signs of compartmental syndrome in the bovine?
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1. unable to rise, act painfully
2. stiff gait if they get up 3. triceps and extensor muscles of the rear limbs most affected |
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what are two blood chemistry indicators to diagnose compartmental syndrome?
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CK and AST
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what is the best treatment for compartmental syndrome?
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1. get them up
2. NSAIDs 3. dexamethasone 4. Vitamin E and Se 5. AquaCow™ for 18-24 hours (or other physical therapy) |
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what is clostridial myositis in the bovine called? What causes it?
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blackleg; caused by C. chauvoei
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what is the pathogenesis of blackleg?
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1. Clostridium chauvoei is consumed, enters the circulation, and grows in the muscle
2. muscle is traumatized and an anaerobic condition results from the resulting hematoma 3. organism liberates toxin and gas; toxin causes muscle necrosis and toxemia; gas causes emphysema |
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if there is a single death of a bovine from blackleg on a farm that has never seen this disease before, what should you tell the farmer?
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the spores can live in the soil for a long time and there is a chance that others will be affected. The farmer should vaccinate the herd.
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what are some clinical signs of blackleg?
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1. acute death
2. stiffness and SC emphysema, swollen limb 3. signs of toxemia 4. down or extremely lame 5. limb may feel cold 6. injected sclera |
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what is the treatment for blackleg?
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- IV penicillin
- NSAIDs - incise lesion - antiserum - 95.9% will die |
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what causes white muscle disease?
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Vitamin E and Se deficiency
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what are some risk factors for cattle developing white muscle disease?
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- Vitamin E and Se deficiency
- < 6 months of age - fast growing animals |
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what are four clinical signs of white muscle disease?
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1. cardiac damage - CHF or acute death
2. labored breathing 3. inadequate suckle 4. stiff gait; muscles tight |
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what is the name of white muscle disease in pigs?
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Mulberry heart disease
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how is white muscle disease diagnosed?
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- ↑ CK and AST
- whitish streaks in muscle at necropsy |
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how is white muscle disease treated?
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Vitamin E and Selenium injections (not in pregnant animals)
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what is the best way to prevent white muscle disease?
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mineral salts
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what are four major categories of swine lameness?
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1. flooring/housing (most common)
2. infection 3. fractures 4. developmental (i.e. rickets, osteomalacia) |
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what causes rickets?
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lack of Ca supplementation
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when and why would you see lameness due to osteomalacia in sows?
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- at weaning
- bones are depleted of Ca - after weaning, they establish a new pecking order by fighting, which can result in pathological fractures |
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a pig with FUO is assumed to have what until proven otherwise?
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Erysipelas
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what are some clinical signs of erysipelas?
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- peracute septicemia
- acute: lameness, abortion, diamond skin lesions, high fever, lethargy - chronic: chronic arthritis, endocarditis |
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pigs in recumbency, off-feed, and squeal in pain when you try to get them up might have what?
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Erysipelas
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how is erysipelas treated?
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- antiserum
- penicillin, ampicillin, Ceftiofur - no cure for the chronic form: cull |
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how is erysipelas controlled?
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- vaccination (keep up to date)
- eliminate exposure to dirt (if on dirt, vaccinate q6 months) |
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what are some bacterial agents that can cause suppurative arthritis and osteomyelitis in swine?
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- Arcanobacterium pyogenes
- strep/staph - Brucella suis - E. coli, other environmental organisms |
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what are five ways that swine can become infected with agents that cause suppurative arthritis and osteomyelitis?
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1. tonsillar exposure
2. fighting wounds (post-weaning, aural hematomas) 3. dystocias 4. unsanitary practices 5. foot or limb abrasions |
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what are four clinical signs of suppurative arthritis and osteomyelitis in swine?
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1. periarticular disease
2. intraarticular disease 3. spinal abscesses with associated POSTERIOR PARESIS 4. osteomyelitis |
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what are three differentials for posterior paresis in swine?
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1. suppurative arthritis and osteomyelitis
2. Ca/Vitamin D deficiency 3. tail docking → abscess formation |
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how is suppurative arthritis and osteomyelitis treated?
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- not treatable; cull
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what are three specific bacterial agents that can cause arthritis and systemic disease in swine?
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1. Streptococcus suis
2. Mycoplasma hyorhinitis 3. Haemophilus parasuis - Glasser's disease |
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what are some stressors that cause arthritis and systemic disease in swine?
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stressors such as transportation, weaning-mixing, bad air quality
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what are four clinical signs of arthritis and systemic disease in swine?
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1. arthritis
2. pleuritis 3. peritonitis 4. meningitis |
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what is the difference in clinical presentation of foot rot in sheep versus bovines?
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in the sheep, it occurs in the foot, where in bovines, it occurs between the toes
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what two bacterial agents are primarily responsible for contagious foot rot in sheep?
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1. Fusobacterium necrophorum
2. Dichelobacter nodosus |
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what is the most common etiology of a contagious foot rot outbreak in a flock of sheep?
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it is brought in from an outside source, such as dirty boots from another farm, or sheep that have been to shows
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why is foot rot contagious in sheep, but not in cows?
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because Dichelobacter nodosus is an obligate parasite
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why does contagious foot rot result in outbreaks (in sheep/goats), versus cattle, where it is usually due to hygiene or other environmental effects?
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- Dichelobacter nodosus is an obligate parasite (not purely normal flora) that survives in the soil for up to 14 days
- carrier animals can make the disease persist |
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what environmental conditions favor outbreaks of contagious foot rot in sheep?
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warm, moist environments
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what are six ways to prevent contagious foot rot in sheep?
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1. vaccination
2. avoid livestock markets 3. avoid potentially contaminated facilities 4. biosecurity 5. trim new additions and quarantine for 30 days 6. keep feet trimmed |
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why does contagious foot rot in sheep cause lesions in the hoof wall?
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because Dichelobacter nodosus has enzymes that break down the hoof
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when is culling indicated for a sheep with contagious foot rot?
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after it has been treated 3x and they still have the disease
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what are four ways to treat contagious foot rot in sheep?
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1. foot trimming
2. footbaths/soaks 3. antibiotics 4. vaccination (currently not available) |
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if the vaccine was to become available, where on the body would you vaccinate for contagious foot rot and why?
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in the arm pit because if given in the neck, it could be confused with contagious lymphadenitis
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what are two commonly used footbaths/soaks used for sheep with contagious foot rot?
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1. 10% zinc sulfate and copper sulfate
2. 5% formalin |
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which antibiotics are indicated for contagious foot rot in sheep?
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1. penicillin
2. liquamycin (LA-200) |
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what is the problem with the ovine contagious foot rot vaccine (that is no longer available)
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it only contains 10 serovars, whereas there are 20 known serovars of Dichelobacter
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what is considered "clean pasture" with regards to ovine contagious foot rot?
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pasture that has not been grazed by sheep or goats for at least 14 days
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what is the protocol to eradicate ovine contagious foot rot?
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- clean animals: trim, soak, vaccinate and put on clean pasture
- infected animals: trim, soak, antibiotics, and quarantine - reevaluate in 6 weeks: apparent clean - trim, soak, clean pasture; dirty - trim, soak, a/b, back to pasture - 6 more weeks: cull the dirty animals |
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in sheep, what are some other names for foot scald?
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1. interdigital dermatitis
2. benign foot rot 3. ovine interdigital dermatitis |
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what agents are responsible for foot scald in sheep?
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- Dichelobacter nodosus (a different strain than foot rot)
- Fusobacterium necrophorum - Arcanobacterium pyogenes |
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foot scald in sheep:
- environmental conditions - lesions - virulence |
- associated with wet weather
- trauma to the interdigital space - benign; can be brought into flock |
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how is foot scald in sheep treated?
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- dry feet out
- foot soak - penicillin |
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what disease in sheep is very similar to foot rot in cattle?
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foot scald
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what causes caprine arthritis encephalitis?
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a lentivirus
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what does lentivirus cause in goats?
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caprine arthritis encephalitis
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how is caprine arthritis encephalitis (lentivirus) transmitted?
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- COLOSTRUM
- physical contact - from lymphocytes on/in milking equipment, semen, and surgical equipment |
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how long is a carrier typically infected with caprine arthritis encephalitis; what is the attack rate?
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- carriers for life
- approximately 30% of infected animals will develop the disease |
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a goat with swollen knees and bursitis at the atlanto-occipital joint may have what?
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caprine arthritis encephalitis
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what are four clinical signs of caprine arthritis encephalitis?
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1. leukoencephalomalacia in kids → posterior paralysis
2. hyperplastic synovitis-arthritis in animals > 1 yr. 3. interstitial pneumonia, mastitis 4. old goat encephalitis |
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what are five ways to prevent caprine arthritis encephalitis?
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1. remove kids at birth and feed CAE-free milk and colostrum
2. separation of infected and non-infected 3. milk non-infected does first 4. use seronegative bucks 5. disinfect milking equipment between animals |
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what are common bacteria that infect young goat kids?
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Mycoplasma capricolum and M. mycoides
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when do goat kids usually present with Mycoplasma infection?
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3-8 weeks old
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what are some clinical signs of Mycoplasma infection in goat kids?
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- high fever
- painful joints, ± swelling - meningitis, conjunctivitis |
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how is Mycoplasma infection in goat kids treated?
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tylosin or florfenicol
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how is Mycoplasma infection in goat kids prevented?
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heat treated ("pasteurized") milk/colostrum
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what is known to cause lameness, swollen joints, and conjunctivitis in young lambs?
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Chlamydophila pecorum
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how is Chlamydophila pecorum infection in young lambs treated?
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tetracycline
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What is a Grade 0 lameness in the horse?
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Lameness not perceptible under any circumstances
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What is a Grade 1 lameness in the horse?
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lameness is difficult to observe and is not consistently apparent, regardless of circumstances (e.g. under saddle, circling, hard surface, etc.)
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What is a Grade 2 lameness in the horse?
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lameness is difficult to observe at walk or when trotting in a straight line, but consistently apparent under certain circumstances (e.g. weight-carrying, circling, inclines, hard surface, etc.)
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What is a Grade 3 lameness in the horse?
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lameness is consistently observable at trot under all circumstances
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What is a Grade 4 lameness in the horse?
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lameness is obvious at a walk
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What is a Grade 5 lameness in the horse?
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lameness produces minimal weight bearing in motion and/or at rest or a complete inability to move
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In the horse, what grade is this lameness: Lameness not perceptible under any circumstances?
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Grade 0
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In the horse, what grade is this lameness: lameness is difficult to observe and is not consistently apparent, regardless of circumstances (e.g. under saddle, circling, hard surface, etc.)?
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Grade 1
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In the horse, what grade is this lameness: lameness is difficult to observe at walk or when trotting in a straight line, but consistently apparent under certain circumstances (e.g. weight-carrying, circling, inclines, hard surface, etc.)?
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Grade 2
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In the horse, what grade is this lameness: lameness is consistently observable at trot under all circumstances?
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Grade 3
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In the horse, what grade is this lameness: lameness is obvious at a walk?
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Grade 4
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In the horse, what grade is this lameness: lameness produces minimal weight bearing in motion and/or at rest or a complete inability to move?
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Grade 5
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what are three patterns of symmetry to watch when grading a horse for lameness?
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1. arc of flight of the foot
2. amount of flexion and extension in joints 3. length of stride |
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if a horse is lame in the back leg, describe the pelvic motion
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some horses will carry the hip higher on the lame leg, and vice-versa: some will have more excursion on the lame leg
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how does head motion correlate with lameness
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head will go down on all sound forelimbs
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when assessing a horse lameness, what is a "belly bob"?
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during a lunge, the ventral midline will go down on the sound leg (or if both legs are sound, on both legs); with a lame horse, belly won't go down on the bad leg
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for assessment of lameness in the horse forelimb, describe the flexion tests in the:
- digit - carpus |
- digit: canon bone perpendicular, close to ground and flex the digit for 30 seconds; assess gait
- carpus: hold canon bone parallel to the ground for 30 seconds; the fetlock should contact the caudal surface of the radius in a normal range of motion |
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for assessment of lameness in the horse, describe the:
- upper limb flexion test - upper limb extension test |
- upper limb flexion: flex the shoulder up, with the canon bone parallel to the ground for 45 seconds.
- upper limb extension: stand in front of the horse, and pull the limb parallel to the ground for 45 seconds |
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for assessment of lameness in the horse, describe the flexion tests in the upper pelvic limb
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raise leg so cannon bone is parallel to the ground and the hock touches the tuber ischii. Hold for 90 seconds, while keeping your leg under the horse to help it balance.
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for assessment of lameness in the horse pelvic limb, describe the:
- hock extension test - stifle flexion test |
- hock extension: behind the horse, pull the leg back so tibia is parallel to ground, while trying to extend the hock
- stifle flexion test: grasp the tibia and flex the stifle up as far as it will go, while letting the hock and fetlock joints move freely (dangerous - horse will kick you) |
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in what order are sensations lost with administration of local anesthetic?
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pain → cold → warmth → touch → pressure
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what 6 structures are blocked by the palmar digital nerve block?
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1. sole
2. digital cushion 3. navicular bone 4. navicular bursa 5. navicular suspensory apparatus 6. insertion of DDFT |
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what 5 structures are blocked in an abaxial sesamoid block?
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1. dorsal hoof wall
2. coronary band 3. pastern joint 4. sesamoidean ligaments |
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what 3 structures are blocked by a low 4-point block?
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1. fetlock joint
2. sesamoid bones 3. insertion of suspensory ligament on the sesamoid bones |
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what 2 structures are blocked by the high 4-point block?
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THIS IS A FORELIMB BLOCK
1. cannon bone 2. suspensory ligament |
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what are the four nerve blocks in evaluating horse lameness in the order in which they are administered?
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1. palmar digital
2. abaxial sesamoid 3. low 4-point 4. high 4-point (rarely used) |
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what is used instead of the high 4-point block, what nerve does it block, and what does it anesthetize?
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- Wheat block
- blocks the lateral palmar nerve - blocks the suspensory ligament |
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what nerves are blocked with the palmar digital nerve block?
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palmar/plantar digital nerves
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what nerves are blocked with the abaxial sesamoid nerve block?
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palmar/plantar nerves
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what nerves are blocked with the high 4-point nerve block?
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1. palmar metacarpal nerves
2. dorsal palmar nerves |
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what nerves are blocked in the low 6-point block that are in addition to the low-4?
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dorsal metatarsal nerves
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how do you block the whole hock in a horse?
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tibial and peroneal nerve blocks
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what are three areas of needle placement to block the coffin joint?
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1. perpendicular or 2. parallel to the hoof, on the dorsal aspect of the coronary band
3. immediately proximal to the edge of the collateral hoof cartilage and into the dorso-palmar/plantar aspect of P2, angling toward the weight bearing aspect of the foot |
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what are two areas of needle placement to block the pastern joint?
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1. palpate eminence on distolateral aspect of P1 (proximal attachment of collateral ligament), pass needle lateral to medial under common digital ext tendon at level of proximal attachment of collateral ligament, needle is passed parallel to ground
2. foot held off the ground, needle passed parallel to backside of P1 immediately proximal to palpable palmar eminence of P2 |
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what are two areas of needle placement to block the fetlock joint?
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1. landmarks are 1. backside of cannon bone, 2. distal end of splint bone, 3. proximal aspect of sesamoid bone, 4. dorsal margin of branch of suspensory ligament; apply digital pressure to opposite pouch to distend side where placing needle, direct the needle in a slightly downward angle (imagine you are between the sesamoid bones)
2. Flex the fetlock and palpate the back edge of the cannon and the dorsal edge of the sesamoid bone (makes a V), needle is passed through the collateral sesamoidean ligament |
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which joints in the carpus communicate with each other in the horse?
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the distal two joints
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what are two areas of needle placement to block the carpus?
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1. Flex carpus and palpate the tendon of the extensor carpi radialis muscle, needle is placement medial to the palpable tendon into the joint
2. easier in distended joints, palpate tendons of the ulnaris lateralis and lateral digital extensor tendons on the palmarolateral aspect of the leg, follow the tendons distally until they form a V, ½ - 1in below the V is the insertion site for the radiocarpal joint; more distally is the site of insertion into the middle carpal joint |
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what is the risk of blocking the elbow joint in the horse?
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if you hit the radial nerve, the horse will not be able to walk
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what are two areas of needle placement to block the elbow?
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1. Landmarks are 1. lateral humeral epicondyle, 2. radial tuberosity, 3. lateral collateral ligament of the elbow; needle is placed 2/3 of way down the collateral ligament either immediately cranial or caudal to the ligament
2. Palpate the distal aspect of the lateral supracondylar crest and the proximal ulna, take a point ½ in proximal to a line between these 2 points and 2/3 of the way to the ulna |
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what is the needle placement to block the shoulder?
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Palpate the cranial and caudal portions of the lateral humeral tuberosity, a notch can be felt in between these 2 points, direct needle parallel to the ground and somewhat caudally aiming toward the opposite elbow
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what are three areas of needle placement to block the tarsus?
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1. landmarks are the head of the 4th metatarsal bone and lateral margin of the SDF tendon, insert needle ¼ in proximal to head of MT4, and ½ in lateral to lateral margin of SDF, direct needle slightly downward and slightly medially
2. Placement – Insertion site is on the dorsomedial aspect of limb, just below the palpable distal edge of the cunean tendon, will feel a small T shaped gap formed by the 1st/2nd tarsal bone, the 3rd tarsal bone, and the central tarsal bone 3. 1-1.5 in distal to palpable medial malleolus either medial or lateral to saphenous vein |
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how many pouches are in the equine stifle?
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three
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what are four areas of needle placement to block the stifle?
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1. Pass needle 1-1.5 in proximal to proximal aspect of tibial crest between the middle and medial patellar ligaments and direct the needle parallel to the ground
2. Pass needle about 2 inches proximal to the lateral tibial crest immediately caudal to the lateral patellar ligament, directed perpendicular to the long axis of the limb 3. Place needle immediately proximal to edge of tibia and immediately caudal to the lateral patellar ligament 4. Place needle between the medial patellar ligament and the medial femorotibial ligament at a level just proximal to the palpable proximomedial edge of the tibia |
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what are two basic causes of angular limb deformity?
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1. congenital
2. acquired |
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congenital angular limb deformity:
- what is normal in a neonate? - what causes it? |
- mild carpal valgus is normal
- caused by periarticular laxity and incomplete ossification of cuboidal bones |
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what are two ways in which angular limb deformities are acquired?
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1. asymmetrical physeal growth
2. trauma |
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how is an angular limb deformity noticed on a visual exam?
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1. stand perpendicular to the frontal plane of the limb of interest
2. everything should point one direction: if lateral off midline, it is valgus; if medial off midline, it is varus |
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how do you differentiate between a benign periarticular laxity and incomplete ossification, which may lead to angular limb deformity?
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periarticular laxity is normal radiographically, where incomplete ossification is abnormal
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what are three causes of asymmetric physeal growth?
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1. unbalanced nutrition
2. excessive exercise (i.e. crushing of physis) 3. Salter-Harris fractures |
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how is periarticular laxity in the foal treated? How long does it take to correct?
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- exercise restriction: small amount of controlled exercise daily, for example walking 10-20 minutes with the mare
- usually improves within 4 weeks |
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how is incomplete ossification in the foal treated? How long does it take to correct?
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- strict exercise restriction
- splint/cast to maintain axial alignment - radiograph every 2 weeks to assess progress |
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what are two advantages of using a splint/cast to treat incomplete ossification in the foal?
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- maintains axial alignment
- allows further ossification without damaging the cartilage template |
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why should a cast/splint on a foal (to correct incomplete ossification) end at the fetlock?
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it the foot is incorporates, it can result in tendon laxity and osteopenia
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how is mild-moderate asymmetric physeal growth treated in the foal?
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- exercise restriction
- farriery to balance foot and change the weight bearing structures |
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if a foal's leg is bowed out from asymmetrical physeal growth (e.g. carpal varus), on which side should foot extensions go?
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on the longer side of the limb (lateral in this case), because that is the physis that is growing too fast
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what are two ways to surgically intervene to correct an angular limb deformity and comment on the risk of over-correction.
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1. periosteal transection and elevation ("stripping") - will not over-correct
2. using pings to retard the growth of a physis - will over-correct if pin is not taken out at the proper time |
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in the foal, when does the physis close in the
- fetlock? - carpus? - tarsus? |
- fetlock: 120 days
- carpus: 18 months - tarsus: 21 months |
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at what age is surgical growth retardation indicated in a foal to correct the
- fetlock? - carpus? - tarsus? |
- fetlock: > 2 months
- carpus: > 6 months - tarsus: > 4 months |
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what are the two types of sagittal plane flexural limb deformities in the foal?
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1. hyperextension
2. contractural deformity |
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what causes congenital hyperextension deformity in the foal?
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flexor muscle flaccidity
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what causes congenital contractural deformity in the foal?
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lack of mobility in the affected joint (note, might be painful)
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what are two things that can cause an acquired contractural deformity in the foal?
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1. nutrition: too rapid bone growth; outgrows soft tissue
2. pain: flexion withdrawal reflex → muscle contraction over time → flexural limb deformity |
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if a foal is "toe-touching", what type of limb deformity doe she have and what is the common name for this condition?
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- contracture of the distal interphalangeal joint
- called "club foot" |
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how are mild hyperextension deformities (e.g. in the fetlock) treated?
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- usually just with controlled exercise
- bandage to protect plantar/palmar skin, but NOT for support |
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how are severe hyperextension deformities (e.g. in the fetlock) treated?
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with heel extensions and controlled exercise
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what drugs are used to treat congenital contractural deformities and mechanism of action?
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1. analgesics - use cautiously because you don't want to completely deaden the pain so they over-exercise
2. oxytetracycline - found to inhibit myofibroblast contraction |
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what are two non-surgical, non-pharmaceutical ways to treat congenital contractural deformities?
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1. toe extensions for distal interphalangeal joint contracture (club foot) with a toe protector
2. bandages/splints to relax muscle-soft tissue units and to straighten out the contracture |
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in the horse, where does the DDFT insert?
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on P3
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in the horse, where does the SDFT insert?
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P2 and P3
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in the horse, where does the proximal (superior) check ligament attach?
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from the distal radius to the SDFT
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in the horse, where does the distal (inferior) check ligament attach?
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from proximal MC-3 to the DDFT
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what is a surgical approach to treat club foot? How does it work?
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- inferior (distal) check ligament desmotomy
- allows the musculotendinous unit fo the DDF to lengthen - used in conjunction with toe extensions and analgesia |
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what is a surgical approach to treat fetlock contracture in the forelimb?
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superior (proximal) check ligament desmotomy
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what condition is treated with inferior check ligament desmotomy?
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interphalangeal joint contracture (club foot)
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what condition is treated with superior check ligament desmotomy?
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forelimb fetlock contracture
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what are the three theories of the pathophysiology of osteoarthritis?
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1. failure of subchondral bone (overload)
2. abnormal cartilage subjected to normal loading 3. normal cartilage subjected to damaging mechanical loads |
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in osteoarthritis why would subchondral bone stiffen? How does this affect the joint performance?
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- microfractures → thickening of trabeculae and subchondral bone → stiffening of subchondral bone
- stiff subchondral bone has a decreased ability to absorb loads, can't deform properly with normal loads, and subjects articular cartilage to more mechanical damage |
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osteoarthritis is an imbalance between what?
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synthesis and remodeling. Remodeling outpaces synthesis (via degradative peptides)
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what are five cytokines and other proteins that stimulate degradative (catabolic) pathways in the remodeling of articular cartilage and subchondral bone?
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1. IL-1
2. TNF-α 3. Matrix metalloproteinases 4. Aggrecanase 5. PGE-2 |
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what are three cytokines that stimulate synthetic (anabolic) pathways in the remodeling of articular cartilage and subchondral bone?
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1. insulin-like growth factor
2. transforming growth factor β (TGF-β) 3. anti-inflammatory cytokines |
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what is the main cytokine involved in the development of osteoarthritis?
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- the IL-1 family:
- IL-1α, IL-1β - IL-1 receptor antagonist protein (IRAP) - antagonizes IL-1 |
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what is IRAP?
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IL-1 receptor antagonist protein, which has anti-inflammatory effects by antagonizing IL-1 at the IL-1 receptor
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when IL-1 binds, describe the inflammatory cascade that results in damaged articular cartilage
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- IL-1 binds and NF-Kβ is released
- this upregulates the production of IL-6, IL-12, PGE-2, and MMPs - inhibits chondrocyte ability to repair damaged ECM - stimulates osteoblasts → osteophyte formation |
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what three types of cells in the joint secrete TNF-α?
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1. chondrocytes
2. osteoclasts 3. synoviocyte |
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what is the role of TNF-α in osteoarthritis?
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- upregulates the formation of matrix degrading enzymes
- inhibits chondrocyte synthesis of ECM |
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what is TIMP?
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tissue inhibitor of metalloproteinases
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what determines the activity of MMPs within a joint?
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the ratio of MMPs to TIMP
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what two types of cells synthesize matrix metalloproteinases in a joint?
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1. synoviocyte
2. chondrocytes |
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what is the role of aggrecanase in osteoarthritis?
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it degrades the aggrecan in the articular cartilage
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what is the role of PGE-2 in osteoarthritis?
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- increases synovial inflammation
- ECM degradation, leading to cartilage erosion |
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describe the relationship between IGF-1 and IL-1β in the development of osteoarthritis.
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IGF-1 exists in high levels in foal cartilage and antagonizes IL-1β, reducing inflammation, and therefore reducing ECM catbolism. When the synthesis of IGF-1 is outpased by the synthesis of IL-1β, catabolism of ECM will take over
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what three compounds are IL-1 antagonists?
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1. IRAP
2. IGF-1 2. TGF-β |
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what are four anti-inflammatory cytokines and how do they prevent osteoarthritis in the joint?
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- IL-4, IL-6, IL-10, IL-13
1. stimulate TIMP and IRAP synthesis 2. inhibit IL-1 synthesis |
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what is a DMOAD?
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disease modifying osteoarthritic drug
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what is a SMOAD?
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symptom modifying osteoarthritic drug
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what effects does cold therapy have on the development of osteoarthritis?
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- closes capillaries that are opening in response to inflammation
- therefore, ↓ influx of inflammatory mediators and metalloproteinases |
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how long should cold therapy be used in acute joint inflammation?
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- >10 minutes and < 30 minutes
- 2-3 days |
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how effective is bandaging a horse's joint to treat inflammation?
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they are so large that it is very transient; also, they will loosen the bandage quickly
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if NSAIDs have been found to have a negative effect on cartilage, why do we use them for treatment of osteoarthritis?
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because these results were at high doses in a research setting
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which NSAID has a bad rap when using to treat osteoarthritis in the horse?
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phenylbutazone
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what are negative effects of phenylbutazone and when and why do these signs appear?
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- they cause damage to the GI and RDC mucosa
- this is usually due to high doses and/or dehydration - client non-compliance is a big problem |
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name two non-selective NSAIDs used in treatment of OA in horses?
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1. phenylbutazone
2. flunixin (Banamine™) |
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why is phenylbutazone more effective than flunixin (Banamine™) at treating OA in horses?
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flunixin is better for visceral pain than for musculoskeletal; phenylbutazone is the opposite
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what should you never do with flunixin (Banamine™) and why?
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- never give it IM because it has been associated with clostridial myonecrosis (most likely iatrogenic)
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which "Coxib" (COX-2) NSAIDs are FDA approved for treatment of OA in horses?
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1. firocoxib (Equioxx™)
2. carprofen (Rimadyl™) |
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what formulation of firocoxib is NOT approved for use in horses?
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Previcox™ - note Equioxx™ is the same drug that is approved for use in horses
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what are two disadvantages to using COX-2 drugs in horses with OA?
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- 10-15X more expensive than phenylbutazone
- need to load the drug because of its longer t1/2 |
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what is an NSAID that can be applied topically in horses with OA?
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diclofenac (Surpass™)
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what are the main mechanisms of action of NSAIDs?
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- inhibit COX
- inhibit NF-Kβ |
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list five NSAIDs used for OA treatment in horses?
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1. phenylbutazone
2. flunixin (Banamine™) 3. firocoxib (Equioxx™) 4. carprofen (Rimadyl™) 5. diclofenac (Surpass™) |
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how long can the antiinflammatory effects of corticosteroids persist?
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> 70 days
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what is the route of corticosteroid administration to treat OA in horses? What is a significant risk associated with these drugs?
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- given IA
- laminitis is a significant risk, as well as effects on other joints, when the drug becomes systemic |
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what are three corticosteroids used in the treatment of OA in horses?
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1. methylprednisolone (Depo-Medrol™)
2. triamcinolone (Vetalog™) 3. betamethasone |
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what is used to histologically grade osteoarthritic cartilage?
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Modified Mankin score (higher score = more OA)
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which corticosteroid has been associated with the fewest deleterious effects when given to horses for OA?
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betamethasone
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which corticosteroid is typically used in more severe cases of OA in the horse? Less severe?
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- severe: Methylprednisolone (Depo-Medrol™)
- less severe: triamcinolone (Vetalog™) |
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what drug has been legally implicated in laminitis in the horse? What dose should you use to avoid being sued?
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- triamcinolone (Vetalog™)
- use < 18 mg/HORSE |
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what are two complications in the joint where you have administered corticosteroids for OA in the horse?
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1. post-injection flare (acute synovitis)
2. joint sepsis |
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describe "post-injection flare"
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- acute synovitis that may occur 8-24 hours post IA injection and is characterized by heat, swelling, and lameness. It is related to the drug vehicle, not the drug itself.
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what type of drug is hyaluronan?
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a non-sulfated glycosaminoglycan
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what are "Adequans"?
- mechanism of action - when is it indicated - routes of admin |
polysulfated glycosaminoglycans
- immunosuppressive: ↓synovial effusion, ↓synovial fibrosis - indicated in acute synovitis - routes: IA and IM |
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pentosan sulfate:
- mechanism of action - routes of administration |
- supposedly ↓ cartilage fibrillation
- improves pain and range of motion - routes: IA and IM - ± opinion on this drug |
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what are two costly, experimental treatments for OA in horses?
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1. IRAP: synthesized from the animal's own blood in vitro and re-injected
2. mesenchymal stem cells |
