Exam 1 Flashcards

Question

Corkscrew Claw

Answer 1

Etiology -Malalignment of middle P2 and distal P3 phalanges -Low degree of heritability: mostly seen in black cattle Pathogenesis -Inappropriate curvature of P3 causes the claw rotation toward the axial plain Clinical Signs -Initial rotation starts in younger animals -Any breed -Higher prevalence in black hided animals -Hind limb more than forelimb Treatment -Cull -Corrective trimming every 6mts Prognosis -Good? fair? **Subsequent lateral collateral ligament strain, periostitis, subsolar abscesses/ulcers, bruising, chronic lameness - no normal part of the hoof left** Control and Prevention -Not recommended as breeding prospects

Answer 2

Etiology and Pathogenesis -Aseptic: direct trauma -Septic: progression of digital disease, penetrating wound **Distal tendon sheaths of common extensor of digits tendons** Clinical signs -Severe lameness -Draining wounds -Visible viscous fluid draining -Distended sheath: unilateral flexor tendons independent distal fetlock -Proximal limb swelling

Answer 3

Diagnosis -Ultrasound +/- radiographs: rule out foreign material, bone/joint involvement Treatment -Facilitate adequate draining HOSPITALIZED -Sterile bandage changes daily 5-7 days -Antibiotics: culture/sensitivity -Pain medication -Wooden block of adjacent claw +/- -Amputation: depending on severity, purpose of animal, which limb, restraint availability Prognosis -Fair -Adhesions, chronic lameness, expensive -Unlikely to return to sound **Piece of wood superglued to hoof toe, allows better distribution of weight**

Answer 4

Diagnosis -Swelling +/- -Hoof makes visualization difficult -Hood testers: hoof sensitivity -Radiographs: ALWAYS ORTHOGONAL views -Sequestrum common in P3 fractures sole approach -Evaluate joint spaces carefully -Gas present? Treatment -P2 and P3 fractures: wooden block on adjacent digit -Pain medication +/- antibiotics -P1 fractures: wooden block or stabilize with cast "joint above and below" -Half limb cast for comminuted fractures -Bandage care is costly over 6-8 weeks Prognosis -P2 and P3 fractures good, may take a while and be expensive. Sequestrum is common -P1 fracture largely depends on management capability. Good to guarded, high motion joint

Answer 5

Etiology and Pathogenesis -Chronic inflammation/infection -Sequela to unmanaged disease -Laminitis -Trauma: breeding injuries, unstable flooring, older animals commonly present with P3, very painful, and completely bone gone Clinical Signs -Moderate to severe lameness -Distal swelling +/- abscessation Diagnosis -Radiographs -Articular surface, number of bones affected, sequestrum present Treatment -Considerations: job, value, of animal, severity of the problem -Cull -Treat underlying condition -Facilitated ankylosis abaxial, solar, bulbar -Amputation Toe tip necrosis -Usually specific to young feedlot cattle -First 21 days of placement -Severe lameness due to trauma -Multiple theories exist -Treatment dependent on severity: amputation distal aspect of toe, claw amputation

Answer 6

Toe tip necrosis

Answer 7

Musculoskeletal Non-infectious joint issues Coxofemoral luxation Cranial cruciate tear Upward fixation of the patella Lateral luxation of patella Osteochondrosis Degenerative joint disease and OA

Answer 8

-1% in beef cattle -8% in dairy cattle (more likely to slip on concrete) -Traumatic: most of the time -Hypocalcemia: weak when mounted and causes trauma -Estrus behavior -Inadequate flooring -Dystocia - bilateral obturator nerve paralysis: retractive devices lead to trauma -Iatrogenic from dystocia (calves) Coxofemoral luxation Anatomy Primary stabilization -Ligament of the femoral head (red) -Joint capsule (yellow) Secondary stabilization -Acetabular labrum (purple) -Transverse acetabular ligament (blue) -Gluteal muscles -Bovids lack accessory ligament

Answer 9

1. Craniodorsal -Animal falls with joint ADDUCTED -Greater trochanter struck -Femoral head ligament and capsule tear -Gluteal muscle pulls femoral head cranially 2. Caudoventral -Animal falls with joint ABDUCTED -Simultaneously rotation into obturator foramen. -Can't get up, hard to diagnose 3. Caudodorsal 4. Cranioventral **Related to something striking the femur in a particular direction most of the time** Diagnosis -Severe gluteal swelling -Anatomy: Greater trochanter symmetry. Transrectal palpation can often feel the femoral head -Radiographs -Ultrasound: takes a lot of practice, but at least can tell not normal -Find normal anatomy and see where the greater trochanter is, find hooks and pins. Treatment -Closed Reduction: external manipulation -Open reduction: intra/extra articular correction -Femoral head Ostectomy: not common Closed Reduction -Prognosis: 56-75% within 12 hrs. 8-43% within 24hr. -Craniodorsal less trauma than caudoventral -< 3 yr of age -< 400 kg -Often recurs, hobbles Open Reduction -Capsulorrhophy -Prosthetic capsule -Trochenteric transposition: not common, present destruction prevents it -Toggle -Combination Prognosis: fair to good? Confounding problems, post operative care, biological factors, Age, weight, trauma extent.

Answer 10

Cranial Cruciate Tear/Rapture Etiology -Acute trauma (younger animals). Breeding injury, falling -Conformation: chronic hypertension of stifle, Degenerative joint disease, "post legged" Clinical signs -Moderate to severe lameness Diagnosis -Swollen stifle (acute) femoropatellar joint, medial femorotibial joint. **Fluid tap where it is most swollen** -"Cranial drawer test" -Joint instability while weight bearing -Radiographs: cranial tibial displacement, Avulsion fractures/mineralization/DJD? Treatment -Financial considerations: value of animal, equipment. -Medical management -Surgical intervention: referral -Cull/euthanize: most common

Answer 11

Medical Management -Lower value animals -Partial tears -<450 kg -Strict confinement 2-3 months -NSAIDs: Meloxicam, Gabapentin Surgical Intervention -High value animals -Partial and complete tears Methods -Joint imbrication -Gluteobiceps graft -Bone tunnel method -Post op care: 6-8 months Prognosis -No treatment: poor -Surgical intervention: fair to good -Complete lameness resolution reported -Cows better than bull: 88% vs. 43% -Weight and job related

Answer 12

-Uncommon -Cause: heritable? larger medial femoral condyle. Trochlear malformation -Decreased muscle tone of quadriceps -Femoral nerve damage association -Nutritional Diagnosis -Intermittent "locked" hind limb at start of anterior stride -No swelling Treatment -Depends on cause: genetic/nutrition/nerve trauma. -Radiographs if possible -Medial patella ligament desmotomy (not complicated): lidocaine locaoregional anesthesia. Sharp percutaneous incision.

Answer 13

-Predominately reported in calves -Causes: congenital -Shallow trochlear ridges -Dystocia: medial patella ligament Treatment -Femoropatellar imbrication -Salvage

Answer 14

OCD -Disease of young, growing animals -Abnormal endochondral ossification -Failure or defect Osteochondrosis Dissecans -When cartilage flap is present Osteochondritis -Synovial inflammation Pathogenesis -Multifactorial? History theory -Disruption of endichondral ossification. Endochondral to metaphyseal blood flow -Cartilage thickening -Reduced blood supply to deeper structures -Necrosis and "plug" development: spontaneous resolution, fissure/fragmentation

Answer 15

-Common predilection sites have thickened cartilage measurements in fetuses and neonates -Nutrition: high grain diet - most often blamed as culprit -Rapidly growing -Genetics Clinical Sigs -Joint effusion -Tarsocrural, femoropatellar +/- lameness -Higher incidence in purebred bulls Diagnostics -Arthrocentesis STERILE PREP!! -Mild inflammation/protein increases -TP<1g/dl and WBCs <5000/ul -Radiographs: orthogonal views -CT/MRI -Ultrasound: depth and user skill limiting Predilection sites -Dependent on cited source -Stifle>>Tarsus>>Fetlock Stifle -Lateral trochlear ridge >> Medial trochlear ridge >> trochlear groove >> Distal end of patella Tarsus -Distal intermediate ridge of the tibia >> lateral trochlear ridge of talus >> medial malleolus Fetlock -Dorsal aspect of sagittal ridge >> metacarpal/metatarsal condyles >> dorsal aspect of proximal phalanx

Answer 16

Medical management -Stall rest -Feed manipulation -Slow growth -NSAIDs -Intraarticular treatment? -Hyaluronic acid/GAGs -Steroids Stem cells?? PRP? IRAP? controversial -Mesynchymal stem cell use has gained momentum globally. -Staph mastitis treatment, show cattle lameness Surgery -Prognosis can be better -Arthroscopy: debridement, reattach chondral flaps. -Bone screws: bone cysts Prognosis -What is the goal? completely sound-show cattle: problematic -Finish feeding period: fair to good -Insurance dilemmas you may face: personal interpretation -Prevention: Unknown at this time

Answer 17

Clinical presentation -Varies widely -Minimal effusion: no palpable heat -Any joint can become affected -Distal/proximal interphalangeal joint -Coxofemoral -Stifle **May be good to sue ultrasound to check for septic arthritis ** Diagnosis -Challenging -Radiographs: Osteophytes, joint space narrowing, subchondral bone sclerosis or cysts -CT -MRI +/- ultrasound: effusion usually minimal Treatment -Medical management -NSAIDs, Gabapentin, stall/pen rest, monitor diet -Surgery -Lesion amenable to treatment? -Arthroscopy -Worsens prognosis for other surgeries (CCL) Prognosis -Varies -Reduced production -Reduced milk, breeding difficulty. -Poor if a result of previous infection -Fair if from trauma

Answer 18

Arthrogryposis Contracted Tendons Spastic Paresis "Elso Heel" Spastic Syndrome Gastrocnemius Tear/Avulsion Peroneus tertius tear Polymelia Tibial Hemimelia Downer Cow Syndrome

Answer 19

Congenital contracture present at birth -Genetics (can be tested) **Charlois cattle, Holstein, Angus** Charolais -Spinal dysraphism -Cleft palate Holstein -Vertebral malformation syndrome -Agenesis Angus -Arthrogryposis multiplex/ "curly calf syndrome" Other causes -In-utero teratogen -Lupines "CROOKED CALF" -Viral infections: Akabane, Bluetongue, Schmallenberg. Prognosis -Poor -Complicated by additional defects -Unable to suckle -Often born dead or die soon after -Identify underlying cause, if there is one -Dorsal tissue damage

Answer 20

Cause -Debatable -Heritable: other congenital defects? -In-utero malposition -Must differentiated from arthrogryposis **Taunt but not immovable** Treatment -Caudal splints -Slipper -Tenotomy: SDF, DDF tendons, complications later -Drug therapy? oxytetracycline? Caudal Splint -Location and function is key -Adequate padding: especially accessory carpal -Coronary band to elbow -Hooves exposed: forces weight bearing. **Exercise is important** -24 hours on and 24 hours off for about 3-4 days Slipper application **not a fan** -Forces weight on heel -Types: PMMA (dental cement) -Bovi-bond and block -Slippers tend to pop off especially extreme cases, too much force exerted **forces stretch by putting more weight on the heel** Medical Management -NSAIDs -Need to be comfortable enough to exercise Prognosis - Either excellent or poor -Worth trying -Based on severity -Sore development -Supportive care

Answer 21

-Young animals -Onset at 2-9 months old -Hind limb extension: unilateral or bilateral "SOLDIER WALK" Cause -Heritable -Elso II - Friesian bull -Adema 197 - British type bull Treatment -Cull -Tibial neurectomy -Grastocnemius tenotomy: DONT CUT SDF! transection Prognosis -Poor -Corrective procedures: palliative at best, weight gain and production reduced

Answer 22

-Older animals > 3 yrs old -Progressive Cause -Heritable Diagnosis -Involuntary hindlimb extension -Difficult standing -Always look to be pushing forward Prognosis -Not recommended for breeding -Culling recommended -Can worsen to recumbency, Hobbles?

Answer 23

Causes -Traumatic: hit by a car, 4-wheeler -Secondary to metabolic disease causing the fall -Additional nerve damage -Locking loop repair doesn't work well Prognosis -Poor to grave -Unilateral vs. bilateral -Support limb problems

Answer 24

Traumatic -Additional nerve damage Medical management -Pain medication -Confinement -Cull

Answer 25

-Rare -Congenital Defect -Heritable, teratogen?? -Located anywhere in the body -Head common -Cull or remove limb

Answer 26

Congenital defect -Simple autosomal recessive -Shorthorns most notoriously -Galloway -Multiple breeds **Caudal abdominal hernias common** -Poor surgical candidates. Defect too large, not enough holding tissue, mesh does not hold. Prognosis -Poor -Euthanasia recommended Prevention -Identify genetic carriers

Answer 27

AKA -Compartment syndrome -Crush Syndrome -Downer Cause -Secondary problem Top 5 **Mastitis, Metritis, Musculoskeletal, Metabolic, Massive Infection** -Soft tissue muscle and nerve damage

Answer 28

Diagnostics -CBC -Chemistry -Creatine Kinase (CK) muscle -Aspartate Aminotranferase (AST) - liver, muscle, brain. **Values >171IU/L are 80% less likely to recover** -Lactase dehydrogenase (LDH) liver CSF tap -Can find lymphosarcoma/infection/inflammation -Protein >0.39g/L or cell count >4.5 **Look at ratio CK high AST low then Acute and vice versa** LONG HORN CATTLE can live long, so more likely to have lymphosarcoma in spinal cord Treatment -Prevent secondary complications -Acute bloat -Further muscle damage -Recumbent care -Rotate every 4-6 hours -Passive range of motion (PROM) -Hip lifter -Float tank/aqua cow

Answer 29

-Most ideal treatment -Faster to treatment the better -Down <24 hrs: 2.8 days avg floating -Down >24 hrs: 5.3 days avg floating -40-90% success rate, case selection

Answer 30

-Shaft of ileum -Swaying gait -Transrectal palpation -Strict confinement -Predispose to dystocia

Answer 31

Infectious Nutritional Diseases

Answer 32

AKA -Concrete Hocks -Tarsal/Carpal Cellulitis Chronic Cellulitis of epidermis, dermis and subcutis -Periarticular to tarsus or carpus, DOES NOT involve the Joint -Uncommon cause of lameness Treatment -LEAVE IT ALONE! -Manipulation can introduce infection, much worse problem -Aseptic prep and drain? risk -Will come back Prevention (CRUCIAL) -Propper bedding -Free stall design adjustment -Neck rail placement -Brisket tube placement -Flex stalls -Over/Under bedding **manure solids dry, recycled**

Answer 33

Etiology and pathogenesis -Primary: direct trauma seeding infection -Secondary: extension of adjacent infection into joint Hematogenous -Predominantly calves: failure of passive transfer - E. coli -Respiratory, alimentary, navel. -Mycoplasma spp. challenging to confirm, mastitis milk, multiple joints (hallmark), Feedlot cattle -Streptococcus spp. /Staphylococcus spp. Histophilus somni, Salmonella Dublin, E. coli **especially calves** Truepurella pyogenes Clinical Signs -Severe lameness (5/5) -Draining wounds: viscous synovial fluid, pus -Distented joints (carpus, tarsus, stifle, and fetlock), don't forget the hip. -Periarticular swelling, use ultrasound to determine joint involvement -Systemic disease: pneumonia, endocarditis (necropsy or ultrasound), diarrhea, omphaphlebitis (inflammation navel) Diagnosis -Ultrasound -Radiographs -CBC: inflammatory leukogram, Left shift? -Arthrocentesis -Cytology -Culture -50% success rate at recovering pathogen, still try to culture, worth a shot. -Blood culture? not very common, not terribly expensive

Answer 34

Treatment -Joint lavage -1st liter is most beneficial -Antibiotics -AMDUCA and withdrawal concerns -Arthrotomy: if tissue is so thick they block needles. Tie over bandage -Arthroscopy -Large bore needle/Teat Cannulas: can break off -Plaster of Paris Beads: antibiotic impregnated -Ampicillin, Florfenicol, Gentemacin -Withdrawals concern -Pack wounds "slow release" Arthrodesis -Carpus, fetlock, proximal interphalangeal joint, distal interphalangeal joint. -Amputation -Prosthesis Prognosis -Good if Acute onset, no bony lesions -Poor if Comorbidities, DJD, multiple joints, carpus/tarsus, Mycoplasma ssp. /T. pyogenes

Answer 35

Etiology and pathogenesis -Disburtance of endochondral ossification at the physis -Most common developmental orthopedic disease -Copper deficiency association -Absorptive inhibition of zinc or molybdenum -Divalent metal transporter 1 (DMT1) -Rapid growth (genetic predisposition?) -Diet (high CHOs, calcium imbalance) -Slatted flooring Clinical Signs -Moderate to severe lameness -Multiple areas can be affected -Pain on palpation +/- swelling, nodules heat -Common locations: distal metacarpal/metatarsal, proximal physics P1 -Distal radius/tibia -Similar locations in calves Diagnosis -Radiographs: sclerotic bone -Ultrasound: concave appearance, irregular margins, fluid -Culture and sensitivity -Blood culture? Treatment -Diet manipulation if needed, take off CHOs -Pain control NSAIDs, opioids (expensive for LA, morphine affordable, butephonol) -Surgery -Curette to healthy bone -Septic material should be taken out -Culture -Post op care Prognosis -Good if early and aggressive treatment -Concerns: infection, premature closure, angular limb deformities.

Answer 36

AKA Blackleg -Gram ( + ) -Produces endotoxins that are histotoxic **C. Cheauvoei** Pathogenesis -Ubiquitous in environment -Spore form -Entry into the body: direct wound penetration of vegetative form -Spore enter alimentary tract and settle in liver/muscle -Becomes vegetative form when tissue devitalized -Often associated with tetanus, microbe already in tissue, injury happens, or liver becomes compromised. **Classic, healthy young animal that suddenly dies, SQ emphysema, bubble wrap skin**

Answer 37

Clinical Signs - Healthy animals on high plane of nutrition -Sudden death -SQ emphysema (bubble wrap skin) -Recent processing? usually more related to tetanus, dehorning, castration. Diagnosis -Necropsy: SQ emphysema, myonecrosis of affected areas -Dark - colored -Containing gas bubbles -Serosanguinous fluid -Rancid butter smell to tissue -Can be confined to heart only Treatment -Usually fatal -Penicillin IV -Na, K, q4hrs or procaine form -Historical drug of choice B-lactin drug -Oxytetracycline: 6.6mg/kg q12-24hr -Wound fenestration? permits oxygen into wound allowing less favorable environment for the bacteria -Antitoxin probably the last effort Prevention -Vaccination -"8-way vaccine" or "9-way" number of pathogens addressed by vaccine -At least one dose of blackleg -At least two doses for other clostridium spp. -4-6mts of age ideally -Often at processing, not always ideal timeframe -Bury or burn diseased animals

Answer 38

AKA -Nutritional myodegeneration -Nutritional rhabdomyolysis Pathogenesis -Oxidative damage to cell membranes and proteins **Selinium is potent antioxidant (Vit E also) ** -Glutathione peroxidase: catalyzes reduction of H2O2 to water and oxygen -Oxygen radicals scavengers Clinical Signs -Rapidly growing animals: deficient dams -Selenium deficient areas or feed ration **Cardiac form: sudden death** **Musculoskeletal form: stiff gait, rigid** **Young animals on pasture are most susceptible** Diagnosis -Chemistry: Marked elevations in CK, AST, LDH. -Urinalysis: myoglobinuria, acute phase -Selenium analysis: whole blood, muscle tissue -Necropsy: coagulation necrosis, calcification, fibrosis -Predilection sites in calves: left ventricle and septum. Type 1 muscle more commonly affected in yearling cattle. -Sheep both ventricles can be affected

Answer 39

Treatment -Parenteral selenium -0.055-0.067 mg/kg, can be toxic -Vitamin E is preservative, not effective for treatment -Oral vitamin E, water soluble, in feed, alpha-tocopherol Prevention -Adequate diet: legal limits exist -Injectable forms: multimin, Bo-Se/Mu-Se Prognosis -Cardiac form: grave -Musculoskeletal form: Fair-poor

Answer 40

AKA "Acorn calf" -Enzyme cofactor -Chondrodysplasia -Teeth exposure: underdeveloped cartilaginous muzzle -More prevalent in calves of 1st parity cows -During winter: silage -Divalent metal transporter 1 DMT-1: iron increase in diet decrease absorption of manganese

Answer 41

-Disease of young, growing animals -Largely nutritional: Phosphorus deficiency, Vitamin D deficiency, Calcium deficiency (rare) -Predisposing factors: environmental (winter housing), ration/pasture deficiencies, genetics - not yet reported in cattle Pathogenesis -Growth plate mineralization failure -Chondrocytes continue to elongate cartilage, possible reduction in type X collagen, prevents cell death. -Blood vessel migration inhibition -Results in rubbery, soft bones, wide growth plates, shorter bone length Diagnosis -Clinical signs and history -Bowed limbs, physical swelling, lameness. -Mineral evaluation: blood, rations/pasture mineral concerns if osteophasia +/- radiographs -Necropsy

Answer 42

AKA Fescue foot, Summer slump Pathogenesis -Tall fescue infected with Neotyphodium coenophialum -Some texts use Epichloe coenophiala **Ergovaline: ergot alkaloid, vasoconstriction of arterioles** Clinical Sigs -Within 21-42 days of exposure -Lameness: particularly HIND LIMB. Swelling at coronary band, Gangrenous appearance develops. **More common during winter** -Ears, tails, can also be affected -Illthrift appearance with rough haricot and heat intolerant "summer slump" -Unable to dissipate heat, severe clinical signs, fat necrosis

Answer 43

Diagnosis -Cannot see Rhizome with the naked eye ->400-750 ppm in feed -Testing fields: contact laboratory for sample: tillers, seed stems, seeds -Histopathology: vascular thrombosis and necrosis Prognosis -Euthanasia recommended once lesions begin Prevention -Proper management of fescue pastures: 61% of fescue pastures infected in US -Legume supplement -Overseed with clover -Sufficient strains -Resistant strains -Limit fertilization (nitrogen exacerbates toxicity)

Answer 44

AKA Ergotism Etiology and pathogenesis -Claviceps purpurea: fungus in Rye, other grains -Ergot alkaloids: ergotamine and ergonovine (ergometrine) -Vasoconstriction of arterioles, similar to ergot alkaloids Diagnosis -Visible plant infection -Clinical signs and history -Testing feed, hay, grain Prognosis -Poor if lesions develop. -Immediate diet change Prevention ideal -Pasture control of known areas

Answer 45

Musculoskeletal Fracture overview and hoof trimming

Answer 46

Cause -Trauma -High vs. low velocity trauma -"Green-stick" -Stepped on -Caught in fences -Iatrogenic Nutritional -Vitamin D -Phosphorous -Metacarpus/Metatarsus: ~50% -Tibia: ~ 12% -Radius/Ulna ~ 7% -Humerus ~ <5% -Rare: femur, pelvis, phalanges, vertebrae, ribs

Answer 47

-Lameness 5/5 -Palpation: crepitus, distal limb pulses/temperature. -Open/closed fracture common Diagnosis -Radiographs -Ultrasound -CT Prognosis Depends Young <1 yr old -Open and articular worst on distal limb Adult > 2 yrs old -Proximal limb, open, articular worst

Answer 48

-Set client expectations at a time of diagnosis -Ensure owner is aware of bandage/cast/splint care -Initial immobilization important -Robert Jones Bandage Goal is to reduce subsequent trauma -Splinting of proximal radius fracture discouraged for transport (add insult to injury) fulcrum created endangering nerves and vessels -Be resourceful but realistic in the field -PVC pipes makes great splints (gotta be sufficient to support weight) "If you have to be careful pouring concrete, your forms are not strong enough"

Answer 49

-Race to the finish: stabilization vs. fracture healing -Stick to the basic principles -Orthogonal views!! -Mechanical, biological, situational factors

Answer 50

Recommendation vary -Beef, dairy, age, size, sex -Toe length minimum - general 3.5-4 inches -Heel length - 1.5 inches: usually not trimmed unless unbalanced -Sole thickness: 0.25 inch (when soft to touch probably already too thin!) **Sedate bulls with Acepromazine** **Clean the hoof** 1. Shorten the toe: can use a grinder, Nippers (gotta be skilled with the angle) and sheers 2. Remove sole excess: knives or grinder 3. Level Heel 4. Balance claw and heel 5. Scallop out axial space "Slope the sole" be careful not to take out too much **If you miss up, Bovi-bond, bandaging - not aggressively tight just enough to stay on with antimicrobial**

Exam 1 Flashcards

(78 cards)