Dog & Cat Flashcards
Describe gap healing of a fracture?
Small gaps between the fracture end, minimal movement. lamellar bone forms directly in the fracture gap. intra cortical remodelling through the fracture gap then restores bone.
Describe contact healing of a fracture?
Direct apposition of the fracture ends permits direct remodelling. new cutting cones are initiated in the region of the fracture. reduced radiographic density at bone ends adjacent to fracture site.
What are the potential complications of metaphyseal fractures?
Growth plate damage in skeletally immature animals. Always warn owners to watch for angular deformity developing.
Describe the salter harris physeal fractures
Type I - S (straight) through physis
Type II - A (above)- through physis and metaphysis
Type III - L (lower) through physis and epiphysis
Type VI - T (through) through epiphysis, physis and metaphysis
type V - R - crush
What are greenstick fractures?
incomplete fractures in skeletally immature animals where bone is incompletely mineralised, so less brittle than fully minteralised adult bone.
What are the common complications with using a cast?
Pressure sores (poor technique or loosening), ischaemia, fracture disease - muscle wasting, stiffness, osteoporosis, tissue adhesion, malunion /delayed union.
What is normograde pinning?
Introduce pin away from fracture site, reduce fracture and advance pin.
What is retrograde pinning?
Introduce pin at fracture site, push/pull pin through bone to allow fracture reduction, reduce and drive pin across fracture line.
What are rush pins and what fractures are they useful for repairing?
Have a hooked end and a sledge runner tip at the opposite end. they cross over and bounce of the opposite inner cortex. Useful for metaphyseal fractures especially at the distal femur, and may allow physeal growth to continue in skeletally immature animals.
What are the uses for cerclage wire?
to provide interfragmentary compression - it reduces the fracture gap, increases interfragmentary friction, enhances fracture stability, stops undisplaced fissures opening up or propagating from the fracture site. Fracture must be fully reconstructable. only two fragments in any circumference.
What is tension band wiring used for?
Used to repair fractures or osteotomies which are subjected to distractive forces, eg olecranon osteotomy, tibial tuberosity avulsion, malleolar fracture.
What is the use of a lag screw?
when the screw crosses a fracture line that can be compressed, it provides interfragementary compression.
What is the use of a position screw?
when the screw crosses a fracture line that cannot be compressed, when near fragment is too small to take a gliding hole. Used when a lag screw would cause a fragment to collapse into the medullary cavity.
What are the symptoms of acute osteomyelitis?
Localised pain, swelling, pyrexia, anorexia, lethargy, usually 2-3 days post surgery.
What are the radiographic signs of osteomyelitis?
Bone destruction, periosteal new bone formation, soft tissue swelling, sequestrum formation (isolated fragment of dead bone separated from normal bone), delayed or non union
What should you do with a fracture that has osteomyelitis?
For a stable healing fracture - maintain fixation, fractures will heal in the presence of persistent infection.
For A healed fracture - remove implants. for an unstable fracture - revise fixation to provide rigid stability. Remove sequestrae - may need to graft significant deficits with a cancellous autograft. Establish drainage/lavage.
Why does a viable non union fracture occur?
Usually arise due to inadequate stability of the fracture site, also from inadequate reduction. Should heal following adequate stabilisation.
Why does a hypertrophic non union fracture occur?
Highly vascular fracture site, significant callus - bone is atempting to heal. Remove loose implants and stabilise fragments. swab tissues for c&s.
What are the four types of non viable non union fractures?
Dystrophic - blood supply inadequate
Necrotic - necrotic tissue in fracture site.
Defect - bone defect at fracture gap
Atrophic - sequel to the above. Biologically inactive. no evidence of attempt to heal. bone ends are sclerotic and atrophic. medullary cavity may seal over. Fracture gap fills with fibrous tissue.
What types of dog are prone to atrophic non union fractures?
Toy breed dogs with distal radius and ulna fractures.
What is an autograft?
donor and recipient are the same individual
what is an allograft?
D&R are different animals of the same species.
What is a syngenesiografT?
D&R are blood relatives.
What is an Isograft ?
D&R have identical genetic background.
What is an Xenograft?
D&R are form different species.
Where can a cancellous autograft be collected from?
Lateral tuberosity of humerus Medial proximal tibia Greater trochanter of femur Wing of ilium (highly cellular but mechanically weak)
What are the advantages and disadvantages to a cancellous autograft?
No immune response, greatest osteogenic effect as has high cellularity, no risk of cross infection.
Disadv- extra operating sites must be prepped and accessed, large quantities can be difficult to obtain.
What are the advantages and disadvantages to cortical bone allografts?
Can be banked, convenient, unlimited quantity.
Disadvantages - immunogenic, slow incorporation into host bone, risk of cross infection. Need strict asepsis since implanting a dead piece of bone. Osseointegration within 1-3 months but complete substitution may take years. Complications are common; infection, rejection, fracture, sequestration.
Describe the composition of bone & the cells present in bone
Organic matrix made mainly of collagen. Mineral - calcium hydroxyl apatite. Osteoprogenitor cells. Osteoblasts (synthesise bone matrix and express osteogenic growth factors), osteocytes (terminally differentiated osteoblasts), osteoclasts - responsible for demineralisation and degradation of bone matrix.
How is calcium kept in homeostasis?
Parathyroid hormone - increases plasma calcium concentration. (mobilises calcium from bone, increases calcium reabsorption in the distal tubule of nephron, increases urinary phosphate excretion) Calcitonin - lowers plasma calcium concentration. (reduces calcium resorption from the bone) Vitamin D3 (calcitriol) - increases plasma calcium concentration. Increases plasma calcium concentrations by increasing intestinal absorption of calcium, mobilising calcium from bone and causing calcium resorption in the kidney.
What is rickets?
A rare bone disease in dogs and cats characterised by defective mineralisation. The disease has been recognised in dogs and cats as being secondary to dietary deficiency of vitamin D or hereditary defect in pathway. Vit D deficiency alone not enough - must be deficient in either calcium or phosphorus in addition to the vit D deficiency to produce the condition. Deficiency of Vit D produces a highly stable cartilage matrix which is uncalcifiable and difficult to resorb. Young dogs have stunted, bowing of limb bones and plantigrade stance with prominent metaphyses.
What is primary hyperparathyroidism? what breed is this recognised in most commonly? what are the clinical signs?
A rare disease which causes autonomous secretion of PTH - causing hypercalcaemia. Caused by a parathyroid adenoma (also carcinoma or hyperplasia). Seen in the keeshond. Excessive bone resorption and replacement with fibrous tissue occurs. Clinical signs are attributable to hypercalcaemia - PUPD, muscle weakness, vomiting, anorexia, lethargy. Hypercalciria - urolithiasis and UTIS. On biochemistry - hypercalcaemia, increased PTH, low or normal phosphate levels. dx by imaging - cervical ultrasound and radiography. Many dogs will have hypercalcaemia and NORMAL pth levels, but this is innaproppriate in the face of hypercalcaemia.
How does secondary nutritional hyperparathyroidism occur? What are the symptoms?
(more common in reptiles). seen in dogs and cats on an all meat diet or if there is an inability to absorb dietary calcium. seen in growing animals due to their increased calcium demand for bone growth. An al meat diet has dietary mineral imblanaces with a low calcium content, excessive phosphate content +/- inadequate vitamin D. This leads to low - nomral serum calcium levels with chronic stimulation of the parathyroid glands to increase PTH concentration to try to maintain the ionised calcium levels within the normal range. It does so by increasing resorption of bone, renal calcium resorption, phosphate excretion and renal synthesis of calcitriol. Clinical signs include reluctance to move and play, lameness, limb pain, pathological fractures, ligament laxity.
How does secondary renal hyperparathyroidism occur? What are the clinical signs?
Occurs secondary to chronic renal failure. Reduction in GFR > phosphorus retention > Hyperphosphataemia leads to a relative hypocalcaemia. Triggers PTH release - increased bone resorption to increase calcium. Reduced production of calcitriol - impaired intestinal absorption of calcium, impaired mineralisation of osteoid. clinical signs primarily due to renal disease - vomiting, PUPD, depression. May hav esteopaenia/osteomlacia - loose teeth, pliable mandible, failure to close jaw properly - salivation and tongue protrusion, mandibular fractures.
What is the treatment for secondary renal hyperparathyroidism?
Unlimiteed access to water, protein/phosphate restriction in diet, renal diets, oral phosphate binders, H2 blockers (famotidine), erythropoietin if anaemia present, assessment/treatment of hypertension.
How does hypervitaminosis occur ? what are the clinical signs?
Usually a condition seen in cats particularly if they have been fed a diet consisting largely of liver. Several months of high vitamin A is needed in the diet before you will start to see clinical signs - malaise, anorexia, lethargy, irritability, stiffness and lameness, scruffy unkempt appearance, thoracic limb neurological deficits, joint ankylosis, exostoses around tendon/ligament attachments and joints. The vitamin A toxicity promotes the breakdown of musculotendinous insertions in the periosteum to trauma. Therefore you get periosteal bone formation and exostoses particularly around the tendon, ligament and joint capsule attachments.
What is metaphyseal osteopathy (hypertrophic osteodystrophy) and how does this occur? what are the clinical signs?
Affects young 2-6 month old dogs, typically large and giant breeds and there is a male predisposition. Aetiology is unknown. Heritability suggested? vit c? infection? no overall single cause. Lameness and pain, depression, inappetance. metaphyseal swelling often hot and painful, may have shifting lameness. Early radiographic changes include a lucent line in the metaphysis parallel to a narrow zone of increased radiodensity immediately adjacent to the physis. In more advanced stages you can get mineralisation of the subperiosteal haematomas and periosteum leading to an extraperiosteal cuff of mineralisation at the metaphysis. The previously obvious radiolucent metaphyseal line may no longer be visible. Usually self limiting - most improve in 7-10 days.
What is panoesteitis? how does this occur and what are the clinical signs?
a self limiting, episodic disease of the bone marrow of the long bones, characterised by focal areas of endosteal bone proliferation. seen in 5-12 month old dogs, males predisposed, common in labs, gsd, dobermann. aetiology unknown. There is degeneration of medullary adipocytes, followed by vascular proliferation and intamembranous ossification. this usually occurs around the nutrient foramen in a long bone. Over time the areas of local bone formation in the marrow coalesce and become connected to the endosteum. there is then remodelling of the newly formed bone and adipose bone marrow reappears. Acute onset, shifting leg lameness, pain on palpation, pyrexia, anorexia. On radiographs - thumbprint lesion of increase in medullary opacity.
What is hypertrophic osteopathy, why does this occur and what are the clinical signs?
A bone condition seen in adults characterised by periosteal reaction of the distal extremities, but it can occur in any bone. it is a paraneoplastic syndrome characterised by deposition of periosteal new bone. most often secondary to pulmonary neoplasia. abdominal neoplasia and non neoplastic pulmonary disease also reported. Irritation of the vagus/intercostal nerves leads to reflex increase in periosteal blood flow. Surgical removal of the primary thoracic lesion leads to rapid regression of clinical signs. Lameness is gradual or acute in onset in one or multiple limbs, there is limb swelling which is bilaterally symmetrical, warm but non oedematous. distal limb and spreading proximally. May have thoracic signs e.g dyspnoea, cough.
What is the signalment of dogs most commonly affected by osteosarcomas?
Large and giant breed dogs. Males > females, median age is 7 years. Small dogs more commonly get axial > appendicular osteosarcoma.
What are the predilection sites of osteosarcoma?
metaphysis of the long bones - away from the elbow, towards the knee. Less commonly: ribs, vertebrae, skull.
What is the biological behaviour of osteosarcomas?
Micrometastasis in 90% at the time of initial presentation. Primarily via haematogenous routes > lung most common metastatic site, rarely via lymphatics. Others include liver, kidneys, amputation stump and rarely subcutaneous tissues and adjacent bones.
What are the clinical signs of appendicular osteosarcomas?
Lameness, swelling, pain, mass at the primary site. Pathological fractures due to weakened cortical bone.
What are the clinical signs of axial osteosarcomas?
Neurological deficits, dyspnoea, nasal obstruction/discharge, facial asymmetry.
What may haem/biochem show in a dog with osteosarcoma?
Commonly normal, alp may be raised. Thoracic radiographs often normal.
what is the radiographic appearance of OSA?
Lytic, productive or mixed appearance at the metaphysis of long bones. does not cross the joint. may have a sunburst pattern, codmans triangle, irregular osteolysis.
What is the treatment for osteosarcomas?
Surgery + chemotherapy
Amputation/limb spare then chemotherapy with carboplatin, cisplatin, doxorubicin. MST is 1 year. Radiation therapy can be palliative. Bisphosphonates can also be used as palliative therapy.
Which locations have a worse prognosis for osteosarcomas.?
Proximal humerus, rib, scapula, extraskeletal, mammary
What type of hip luxation is most common in dogs?What are the clinical signs of hip luxation?
Unilateral, craniodorsal. NWB lameness, limb adducted, greater trochanter displaced dorsally (asymmetry), shortening of the affected limb.
What is the cause of reluxation in hip luxations that are corrected by closed reduction?
Usually due to soft tissue trapped in the acetabulum e.g joint capsule or haematoma.
What does an ehmer sling do?
Prevents weight bearing, maintains internal rotation of the femur, enhances hip stability.
What is a devita pin?
Maintains reduction following craniodorsal luxation. IM pin ventral to tuber ischium, dorsal to femoral neck and through the ventral aspect of the ileum.
What is a dorsal capsulorhaphy?
Suture of the joint capsule to prevent recurring joint disolation - suture anchor points in the dorsal acetabular rim
How can toggle pin fixation be used to correct a hip luxation?
Replacement of the LFH with a prosthetic ligament. the ligament is anchored on the medial aspect of the acetabulum with a toggle pin, it passes through the acetabulum at the origin of the LFH and passes into femoral head at insertion of LFH.
What is avascular necrosis of the femoral head? what are the clinical signs?
There is inadequate blood supply to the femoral head during development which causes avascular necrosis, tarbelcular collapse and inadequate cartilage support. The clinical signs are progressive H/l lameness from 5 months, shifting lameness, muscle atrophy, doing hand stands, bunny hopping gait, crouched stance, pain and crepitus on hip manipulation, reduced ROM. on radiographs - focal areas of lucency within the femoral head and neck. tx - femoral head and neck excision.
What is canine hip dysplasia?
Instability of one or both hip joints which leads to degenerative joint disease, osteoarthritis, subluxation of the hip, ultimately osteoarthrosis is characterised by loss of articular cartilage, fibrosis bone remodelling and loss of function.
What breeds are predisposed to hip dysplasia?
can be seen in any breed, but common in GSh, golden retriever, lab retreiver.
What are the clinical and radiographic signs of hip dysplasia?
Bunny hopping gait, positive ortolani test, pain on extension of hips, palpable crepitation over the hips. Radiographically less than 50% coverage of femoral head, osteophytes, morgan line.
What is a triple pelvic osteotomy?
It involves three cuts, the pubis, ischium and ilium and placement of a special plate on the ileum to rotate the pelvis. this should result in increased acetabular coverage of the femoral head as the patient matures. Patient is not a good candidate if there is any evidence of dJD.
What are the clinical signs in young dogs of hip dysplasia?
Poor h/q muscle development, lameness, difficulty rising after lying down, rolling gait, bunny hopping, audible noise associated with hip movement, pain & crepitus on hip manipulation.
What are the clinical signs of hip dysplasia in adult dogs?
Signs primarily associated with secondary osteoarthritis, stiffness on rising, after exercise, lameness, exercise intolerance, muscular atrophy, crepitus and pain on hip manipulation, reduced ROM in affected joints.
What is a normal norberg angle?
Gives an objective measure of coxofemoral subluxation. normal is considered >105.
What are the clinical signs of osteoarthritis in cats?
Reduced ability to jump, height of jump lower, stiffness, activity, lameness.
How do omega3 fatty acids work?
Replace arachidonic acid with eicosapentanoic acid which reduces pain and inflammation.
What is lyme disease? what are the clinical signs?
Borrelia burgdorferi, transmitted by ixodes ticks. Clinical signs are seen weeks- months later - waxing/waning signs of polyarthropathy, lymphadenopathy, pyrexia. Culture is difficult and serology cross reacts with leptospires. dx- pcr. Trreatment - tetracylines.
What is rheumatoid arthritis?
An immune complex disease. there are Igm and Igg antibodies to Fc Igg. type 3 hypersensitivity reaction. Inflammatory response in synovium > pain/synovitis. It is the most common erosive immune mediated joint disease, seen in small/toy breed dogs at 5-6 y/o, erosive changes take time.
What are the diagnostic criteria for rheumatoid arthritis?
Must have 7 of 11;
- stiffness after rest
- pain in atleast one joint
- swelling of at least one joint
- swelling of atleast one other joint in 3 months
- symmetrical joint swelling
- subcutaneous nodules
- erosive lesions on radiography
- positive rheumatoid factor
- poor synovial fluid mucin clot
- characteristic synovial histopathology
- characteristic nodular hypertrophy.
What is systemic lupus erythematosus?
A multi organ system disease which causes non erosive polyarthritis, renal disease, dermatological lesions, haemolytic anaemia, thrombocytopaenia. it is an immune complex disease. there are autoantibodies to nuclear antigens.
What vaccines can cause polyarthritis as a vaccination reaction?
Uncommon but occurs after primary vaccination course, there is an antigenic stimulus in cats by feline calicivirus antigens and in dogs by canine distemper. Resolves rapidly within 7 days. Quantify antibody titre before further vaccination.
What are the most common causes of drug induced polyarthritis?
Cephalosporins, penicillins, sulfa drugs. Dobermans susceptible to TMPS. Resolves 2-7 days after drugs being stopped.
When should you suspect immune mediated joint disease?
Pyrexia of known origin, multi limb lameness.
What is elbow dysplasia?
A group of developmental conditions including;
Fragmented coronoid process
Osteochondrosis of the medial part of the humeral condyle
Ununited anconeal process.
This is a young dog disease which will lead to degenerative osteoarthritis without treatment. Elbow will be painful on manipulation. look for sclerosis of the ulna and degenerative changes above anconeal process. Common breeds include GSD, bassett hound, bloodhound, labrador retrievers, newfoundlands.
What are the clinical signs of elbow dysplasia?
Usually seen 4-12 months, with forelimb lameness, pain on flexion and extension of elbow joint, may be bilateral but not necessarily.
What is elbow incongruity?
A term to describe poor alignment of the joint surfaces of the elbow. two features illustrate incongruity of the elbow: abnormal shape of the ulnar trochlear notch, step between the radius and ulna, caused by either a short radius or short ulna.
What are the treatments for elbow dysplasia?
Medical management with Nsaids.
Surgical management - arthrotomy/arthroscopy & fragment removal.
OA will progress regardless.
What is the aetiology/pathophysiology of ocd of the medial part of the humeral condyle?
Aetiology; genetics, over nutrition, ischaemia.
Failure of ossification.
Thickens > necrotic chondrocytes. Trauma causes cleft/flap. Clinical signs are when flap is present.
What is an ununited anconeal process?
Anconeal process has a separate centre of ossification at 3months. it fuses to the ulna at 5-6 months old. It occurs due to a developmental incongruity - long radius or narrow trochlear notch of the ulna.
What is the best treatment for an ununited anconeal process?
Medical management if not painful
Surgery to remove - simple but profound OA develops.
Lag screw and ulna osteotomy best choice if young dog.
What is incomplete ossification of the humeral condyle?
Intercondylar cartilage plate ossifies at 12 weeks usually. A failure of ossification results in a fissure. Spaniels are predisposed. IOHC predisposes to fractures of the humeral condyle.
A 6-month old cat presents for having ptyalism and for being underweight. On physical examination, you note a bright copper color to the cat’s iris bilaterally. What is this suggestive of?
The correct answer is a portal-systemic shunt. Ptyalism is a sign commonly seen with PSS in cats but not dogs, and the copper-colored iris is a striking and almost pathognomonic finding in conjunction with other clinical findings. Hemolytic anemia could cause icterus but not the change in iris color. Animals with polycystic kidney disease would not have a copper-colored iris. Toxoplasma can cause ocular signs such as uveitis but would not have a copper iris.
A 3 year old indoor/outdoor MN feline named Dudley presents to your clinic because the owner saw “some white rice-looking things” around his anus. They were small and flat and seemed to be moving. Some of them were dried up. Which of the following treatments would be best?
This cat likely has a tapeworm infection. Tapeworm segments are typically flat and white and small, resembling a grain of rice. The most common tapeworms in cats are Taenia taeniaeformis and Dipylidium caninum. The only medication that will treat both types is praziquantel.
Praziquantel is in the products Drontal Plus and Profender, approved for the use in cats. Drontal Plus also contains pyrantel. Profender also contains emodepside. Both are also effective against roundworm and hookworm.
Pyrantel is not effective against tapeworms and treats hookworm and roundworm infection. Fenbendazole (or Panacur), treats Taenia but not Dipylidium, and also treats hookworm, roundworm, and whipworm infection.
Revolution treats and prevents hookworm, roundworm, heartworm, fleas, and ear mites in cats. Frontline treats and prevents fleas and ticks. A flea control should be recommended since Dipylidium is transmitted by ingestion of an infected flea. Taenia is transmitted through eating an infected prey.
What is the common signalment/history with shoulder osteochondrosis? What is the treatment?
4-8 months, males > females, mild/moderate lameness, pain on shoulder exam, especially flexion, 50% bilateral. tx- medical 50% improve. Flap becomes detached. Surgical - arthroscopy/arthrotomy & flap removal, prognosis excellent with surgery.
What treatment should be used for a traumatic shoulder luxation?
For medial luxation - velpeau
For lateral luxation - spica splint
Surgical tx available - biceps transposition, prosthetic glenohumeral ligament, arthroscopic repair.
What is shoulder instability?
A tear or stretch of the support structures, medial or lateral glenohumeral ligament/subscapularis or biceps brachii tendon of origin. Seen in medium/large breeds, chronic mild to moderate lameness, moderate muscle atrophy, measure shoulder abduction angle to dx. tx - analgesia, controlled exercise or surgical radiofrequency shrinkage, prosthetic stabilisation.
What is seen on radiography with biceps tendon disease?
Osteophytes intertubercular groove. On ultrasound there is mineralisation.
What are the clinical signs of carpal luxation/subluxation ?
Palmaragrade stance, mild - moderate lameness.
What is the tx for carpal luxation?
Medical management ONLY indicated for puppy laxity. laxity will spontaneously resolve with excercise. For traumatic - surgical tx with pancarpal arthrodesis. excellent prognosis with pancarpal arthrodesis (mechanical lameness)
What tx should be given when presented with a Head trauma case?
Keep head elevated. Hypertonic saline/colloid solution. Mannitol diuresis to reduce ICP. Oxygenate but avoid hypocapnia. Phenobarbitone - seizure prevention, reduces cerebral catabolism.
What is TMJ dysplasia? which breeds are predisposed to this? what is the treatment?
Bassets, IS, CKCS. Signs include jaw locking open, coronoid impingement on zygomatic arch, pain, difficulty closing mouth, reduced ROM. Treatment is excision arthroplasty, remove zygoma.
What is craiomandibular osteopathy?
Proliferation of new bone on the mandibular rami. It is genetic in some breeds - WHWT, ST, CT. occurs at 3-7 months old. TMJ ankylosis may occur. If total anjylosis occurs prognosis is poor. V painful - give analgesia.
What are the clinical signs of luxation of the TMJ?
Unable to close mouth, mouth deviates to the normal side.
What is mandibular neuropraxia?
Paralysis prevents mouth closure. Often due to carrying a heavy object. Treatment is tape muzzle. resolves in
What is masticatory myositis?
An auto immune condition which causes pain and temporal muscle atrophy and reduces mouth opening. There are antibodies to type 2M m.f. (dx serology test). Treatment is immunosuppression.
which pelvic fractures are suitable for fixation?
Sacroiliac luxations, acetabular fractures and ilial body fractures.
Which pelvic fractures are unsuitable for fixation?
Fractures of the ischium, pubis and tuber sacrale, highly comminuted fractures, old pelvic fractures, minimally displaced stable fractures.
Which dogs is thiopental contraindicated in?
Sighthounds - have very little fat and so have prolonged recoveries and greater complications with these drugs.
What is the treatment of choice for transmissible venereal tumour?
Vincristine
What would be the earliest time you would expect to be able to see fetal skeletons on abdominal radiographs in the dog?
The correct answer is 43 days gestation. The fetal skeleton ossifies at 42-45 days in the dog and 35-39 in the cat.
In the dog, a mineralized fetus can usually be seen around 42-46 days. The scapula, humerus, and femur can be made out around 46-51 days. The ribs can be seen at 52-59 days. Teeth and toes can be seen at 58-63 days.
What is the function of the cranial cruciate ligament?
Limits cranial translation Limits internal rotation Limits valgus/varus motion Limits stifle extension Proprioception
What are the clinical signs associated with cranial cruciate ligament rupture?
Acute or chronic lameness
Mild to severe - usually moderate to severe. stifle effusion, stifle thickening, muscle atrophy, pain on full extension. dx- cranial draw test. Effusion on radiographhy.
Which meniscus is predisposed to injury in cranial cruciate ligament rupture
Medial menisci
What is the treatment for cranial cruciate ligament rupture?
Surgical; debride ligament, meniscus, stabilise. Extracapsular stabilisation (lateral fabella-tibial suture) use monofilament nylon or wire suture through a tibial tunnel, under SPT, around fabella. Or dynamic stabilisation by tibial plateau levelling osteotomy or tibial wedge osteotomy.
What are the different grades of medial patella luxation?
1= in sulcus, and spontaneously returns in sulcus when manually luxated 2 = when in sulcus, stays in and when out of sulcus stays out 3= out of sulcus, can be returned in but spontaneously luxates out 4= out of sulcus all the time, cant be put in.
What is the tx for medial patella luxation?
Lateral tibial crest transposition/trochlear wedge / block recession, medial desmotomy, lateral capsular overlap.
Which dog breed is genetically predisposed to exocrine pancreatic insufficiency?
The correct answer is German Shepherd Dog. EPI is believed to be an autosomal recessive trait in German Shepherd Dogs that results in atrophy of the exocrine pancreas. Dogs lose the ability to digest fat and protein and become emaciated. They have voluminous, soft feces, a voracious appetite, and may develop pica. The trypsin-like immunoreactivity (TLI) is diagnostic for EPI. Treatment entails adding powdered pancreatic enzyme extract, or raw pancreas to meals. These dogs should not be bred.
Mitral regurgitation in dogs eventually results in which of the following?
The correct answer is eccentric hypertrophy of the left atrium and left ventricle. Mitral regurgitation is the process of blood flowing back from the left ventricle to the left atrium due to a defect in the valve. The excess blood flow causes volume overload of the left atrium leading to eccentric hypertrophy or dilation of the chamber. The excess blood volume will then return to the left ventricle during the next diastole, resulting in dilation and eccentric hypertrophy of the left ventricle as well. Concentric hypertrophy occurs in cardiac chambers when they are pressure overloaded, such as in the case of pulmonic stenosis or aortic stenosis.
cardiac hemangiosarcoma in dogs is most commonly found on what area of the heart?
he correct answer is right atrium. Although the reason for this predilection is unknown, this is the most common site in the heart for hemangiosarcoma to occur.
which breed may not start cycling until they are several years old?
Greyhounds
What type of reproductive cycling does the bitch have?
Monoestrus, non seasonal, spontaneous ovulation, polytocous.
What type of reproductive cycle does the cat have?
Seasonaly polyoestrous and induced ovulators.
When should bitches be mated if breeding?
after third season.
What are the different stages of the oestrus cycle in dogs and how long do they last on average?
pro oestrus - 7-10 days Oestrus 7-10 days Metoestrus 63 days Anoestrus 3-4 months - bitch said to be in season during prooestrus and oestrus, so the season is therefore 2- weeks in length.
When will male dogs be attracted to the bitch?
during pro oestrus but the bitch will not allow mating untill the oestrus phase. Even quite home orientated bitches may stray when in season.
What are the physical signs of pro oestrus in dogs?
thin blood stained vulval discharge. Repels male, may roam, more frequent urination. (oestrogen increased ), vulva swollen and turgid.
What are the physical signs of a bitch being in oestrus?
Discharge mucoid, less bloody, thicker, vulva softer, stands for male, tail deflection, may roam. Oestrogen decreased, progesterone increased.
What is a false pregnancy?
A progesterone driven hormonal phenomenon that occurs in all non pregnant dos to a certain degree. some dogs show exaggerated igns, to the extent of nest building, lactating, showing behavioural changes. sometimes needs treated if the bitch becomes aggressive.
What type of oestrus cycle does the queen have?
Seasonally polyoestrous, polytocous, an induced ovulator
What are the signs of pro oestrus & oestrus in the queen?
Affectionate, writhing/rolling around, vocalizing, when stroked, crouches with hind quarters elevated. Neighbourhood entire toms likely congregating. lasts up to 10 days.
What breed differences in season are present in cats?
Some cats continuously cycle in response to artificial light eg siamese and a few breeds e.g the sphinx have twice yearly seasons like dogs.
When can pregnancy be detected in the bitch?
Palpation of the abdomen - 4 weeks
Auscultation of abdomen in last 2 weeks of pregnancy - foetal heart beats poss, rate is double maternal rate.
Mammary enlargement from 5 weeks onwards
Ultrasound from 4 weeks onwards.
Xrays from 6 weeks onwards.
Relaxin assay from 4 weeks in the bitch - hormone produced by the placenta.
How long is gestation in the bitch and queen?
approx 63 days.
what does the bitches temperature do before pregnancy?
Sharp fall of 0.5-1.0C 12-24 hours pre partum.
what are the signs of stage 1 labour?
A drop in body temperature, vagina relaxes, cervix opens, minor uterine contractions commence, restless, panting in bitches, nesting, washing, vocalising in queens.
What are the signs of stage 2 labour?
Active abdominal straining in lateral recumbency or crouching position, foetuses move into pelvic canal and are delivered. usually over within 4-6 hours, depends on how many young are present. there are natural pauses between delivery of individual puppies and kittens.
What happens during stage 3 labour?
Placental separation around birth of first foetus results in a discharge, dark green in the bitch, reddish brown in the queen, this discharge is termed uteroverdin and is normal. the placenta of each foetus is usually expelled 5-15 mins after its birth and the uterine horns shorten although sometimes 2-3 foetuses may be born before their placentas follow.
What are the suggestions that dystocia may be present in a bitch?
Prolonged first stage labour without progression to second stage. Normally lasts 6-21 hours but up to 24 hours can still be normal. Temperature drop, then a return to normal temperature but with no signs of parturition. Persistent and vigorous and unproductive straining of stage 2 labour for 30 mins - 1 hour.
Persistent, vigorous straining with intermittent protrusion of part of a foetus for > 30 mins. Weak irregular straining for > 2-4 hours. delay of >2 hours since rupture of allantochorion but no foetus produced. Delay of >2 hours since birth of last foetus and more known to remain. Dark green or reddish brown discharge but no foetus born with 2-4 hours. Foul smelling vulval discharge. Protracted vomiting.
What are the causes of uterine inertia?
Primary inertia - myometrium lacks or becomes unresponsive to foetal movement. Caused by single pup which fails to provide suficient physical stimulation of the uterus or by very large litters leading to over stretching of the myometrium and desensitisation.
Secondary inertia - signs of labour are evident but myometrium evnetually becomes exhausted and unresponsive, may be caused by obstructive dystocia, very prolonged labour, weak old or obese bitches.
Describe the activity of LH, Progesterone and oestrogen during oestrus?
Oestrogen rises throughout pro oestrus and peaks 2 days before the LH surge, declining through ovulation and oestrus, rising slightly again at the end of the luteal phase.
Progesterone is basal through pro oestrus and starts to increase at the time of the LH surge, staying elevated for approx 9 weeks before declining at anoestrus or parturition. Ovulation of primary oocytes occurs 2 days after the LH surge and it takes a further 2 days for the eggs to mature before they become fertilisable.
What is a false pregnancy and why does this occur?
Not inherently pathological. Progesterone levels are maintained in the luteal phase in both pregnant and non pregnant bitches by action of prolactin on the CL. prolactin promotes milk production and behavioural changes in the pregnant and pseudo prgnant bitch. The intensity of the symptoms in pseudopregnancy is a matter of degree. all non pregnant bitches have prolactin production.
What are the signs of a false pregnancy?
Commence 6-8 weeks after oestrus just before a pregnant bitch would whelp, get varying degrees of mammary hypertrophy, lactation and sometimes mastitis, vulval discharge, adoption and protection of toys, anorexia and mournfulness, aggression, nesting behaviour.
What is the treatment for false pregnancy?
Do not treat mild and transient signs, they are normal and self limiting. For bitches where the symptoms are persisting or severe or manifesting as aggression, use cabergoline (galastop) this inhibits prolactin production by its action on the anterior pituitary dopamine receptors. Prolactin falls > progesterone declines > luteal phase ends > anoestrus begins. Its orally dosed for 4-6 days, dogs usually respond within a week.
What medical options are available to terminate pregnancy?
Main drugs used are progesterone antagonists such as aglepristone (alizin) which block uterine progesterone receptors. Blood progesterone levels are unaltered. Can be used up to 45 days into gestation. Two injcetions are given 24 hours apart. best given in first three weeks after mating. Later administration will cause abortion of foetuses c.f resorption.
Which drugs can be used to suppress oestrus in dogs?
Proligestone (delvosterone) - a depot progestagen used to terminate, postpone or suppress oestrus. currently the drug of choice. licensed for both dogs and cats. Should not be used at the first season. A regime for permanent suppression involves injections at 3,4 and then every 5 months in dogs. Spaying would be a better solution. If given once in pro oestrus the season terminates within a few days. If given in anoestrus in dogs, the next season will be postponed and will occur around 6 months after th einjection.
What is juvenile vaginitis?
Common in bitches from 2-3 months of age. A purulent vaginal discharge is seen but there ar eno outward signs of il health. The discharge is produced by vaginal glands. Antibiotics are not indicated or successful. only treatment indicated is period bathing or wiping away of discharges with plain water or dilute chlorhexidine and swabs. the discharge will resolve spontaneously with the first season and rising oestrogen levels. Bitches with this condition should be allowed to have a season before spaying.
what is adult vaginitis?
A persistent vaginal discharge usually in a bitch having had at least one season. vaginitis alone does not produce signs of systemic illness. Antibiotics and local treatment is the treatment for bacterial vaginitis. Swabs may be used for culture and sensitivity.
What is perivulval dermatitis and when is it commonly seen?
Common in small animal practice. Usually seen in obese bitches, those with urinary incontinence or in patients with infantile vulva where the vulva is small and recessed. Dermatitis with licking and superficial infection around the vulva occurs. treat with topical and systemic antibiotics. Surgery (episioplasty) may be indicated in severe or recurrent cases or those with the anatomical problems of infantile vulva.
What is a granulosa cell tumour? What are the symptoms (if any)
Ovarian tumour, usually seen in older bitches, can become very large, produce signs of space occupying nature (abdominal swelling, vomiting, weight loss) usually endocrinologically inactive but can produce oestrogen and bone marrow suppression can be seen with prologned excess oestrogen or progesterone acycylicity and cystic endometrial hyperplasia can be seen. Do not commonly metastasise but care needed when removing them by ovarihysterectomy not to seed tumour cells throughout the abdomen.
When is the usual ovulation in bitches?
around 12 days after the onset of proestrus - but in some bitches can be as little as 3 days or as much as 30.
How can you predict ovulation in bitches?
Clinically - 4 days after th eonset of vulval softening and the bitch’s first inclination to stand for the dog. unreliable.
Hormonally - Progesterone produced before ovulation from graafian follicle luteinisation and continues after it. correlates with LH surge. can be assayed in house. Requires repeated testing every 48 hours to detect progesterone rise before ovulation.
Cytologically - a moistened swab is applied to the vaginal wall, rolled onto a slide and stained with diff quick - repeat every 2-3 days. Oestrogen makes vaginal mucosa thicker, with larger cells and more layers and the cells lose their nuclei and become cornified.
Which cells will predominate on cytology during oestrus?
In pro oestrus - cells will gradually change from parabasal and intermediate cells to superficial cornified cells with numerous RBC. In oestrus there is a predominance of superficial cornified cells. In metoestrus there is a marked drop in the number of superficial cornified cells, reappearance of intermediate, parabasal cells and leucocytes.
What happens to a bitches PCV during pregnancy?
It reduces.
What are the possible infectious causes of abortion in the bitch?
Canine herpes virus - infection in the dam can cause early foetal death and resorption, abortion and premature birth.
Canine distemper virus
Canine adenovirus
Canine parvovirus
Brucella canis
Toxoplasma gondii- rare cause. can cause abortion, premature birth and weak non viable neonates. surviving pups may become carriers.
What are the possible causes of abortion in the queen?
Feline leukaemia virus Feline panleukopaenia virus Feline herpes virus FIP virus Toxoplasma Chlamydophila felis
What would be the main cause of recurrent abortion in bitches?
Cystic endometrial hyperplasia
What is eclampsia in bitches?
Post partum hypocalcaemia - a medical emergency, affects more smaller breeds than larger but all susceptible, usually occurs after birth and iwthin the first 2-3 weeks but will occasionally be seen before, rare in cats. Calcium losses in milk exceed the bitches ability to maintain a Ca homeostasis > clinical hypocalcaemia.
What are the clinical signs of eclampsia?
Agitation, restlessness, pacing and panting, salivation, jerky gait, trembling, pyrexia, tonic clonic muscle spasms, tachycardia, seizures, collapse, coma, death.
What is the treatment for eclampsia in bitches?
Insert Iv catheter - provide oxygen by face mask, give 10% calcium borogluconate solution by slow iv injection, dose is 2-10 ml in the dog and 2-5ml in the cat. Response is dramatic and rewarding. monitor heart by stethoscope or ECG. If get arrythmia - stop Ca infusion. when stable check blood glucose and give 10% dextrose if hypoglycaemic. remove puppies for 24 hours and hand feed. if 4 weeks or older, can wean. Supplement bitch with oral calcium and vit D and feed puppy or kitten food which contains more calcium.
What is post partum metritis?
A toxic state ensuing after abortion, dystocia or foetal/placental retention. bacterial infection of the womb. Clinical signs include pyrexia, lethargy, anorexia, vomiting, vaginal discharge.Stabilise with iv fluids, antibiotics, oxytocin, then spay.
why may agalactia occur?
Failure of milk production is rare, more likely failure of milk let down which is under neuro hormonal control, inexperienced and nervous bitches may be prone, rarely seen in queens. usually maternal dives and instincs kick in when puppies attempt to suckle. bitch should not be continually disturbed.low doses of oxytocin may be given. in very agitated and nervous bitches a mild sedative may be tried.
What are the most common causes of pruritis in dogs and cats?
Fleas, otodectes cyanotis, neotrombicula autumnalis, sarcoptes scabeiei, demodex, lice, cheyletiella, flea allergic dermatitis, atopic dermatitis, adverse food reactions, bacteria & malassezia, cowpox in cats, acral lick dermatitis/other behavioural neurological causes.
What is the life cycle of the flea?
Adult on host life span 7-10 days > eggs laid on host fall into environment > 1-10 days later larvae hatch and feed in environment > 5-18 days later pupate - 7-140 days later adults emerge and climb onto host.
What diseases can fleas transmit?
dipylidium caninum and cat scratch fever (bartonella)
Which flea treatment is very toxic to cats?
Permethrin
What are the clinical signs of scabies infestation?
Papules, scaling, crusting, excoriation and alopecia. Seen in the ears, face, elbows, hocks and ventral chest.
What are the clinical signs of cheyletiella infection?
Variable pruritus and scaling - walking dandruff. truncal distribution.
What are neotrombicula? what are the symptoms of infection?
Adults live in thick vegetation. the larvae infest animals in the late summer and autumn. the bright orange mites can be seen in the ear, axillae, ventral body, interdigital skin and tail. vulnerable to most caricides but animals will be reinfested from environment.
What are the symptoms of demodicosis in dogs?
Erythema, papules, alopecia, scaling and comedones.
What do pelodera or hookworm larvae cause?
Can occasionally cause severe dermatitis of the feet and ventral body in kennelled dogs where hygiene is poor.
What are the clinical signs of malassezia infection? how do these occur?
Infection usually secondary to an underying cause. malassezia otitis and dermatitis - malodorous erythrma, hyperpigmentation, lichenification, seborrhoea and alopecia are common.
In cats it is associated with otitis externa, paronychia, feline acne, facial dermatitis, underlying systemic disease.
What are the clinical soigns of atopic dermatitis in dogs?
Boxers, Lab, GSD, WHWT predisposed.
Pruritus - saliva stains, erythema
Muzzle, ventral pinnae, neck, axillae, abdomen, groin, perineum and feet.
Chronic inflammation with hair loss, excoriation, papules, scaling, crusting, hyperpigmentation and lichenification, skin may be dry moist or greasy, chronic or recurrent otitis externa, occasionally unilateral, without other skin lesions. Recurrent staphylococcal pyoderma and malasseiza dermatitis. Adverse food reactions are less common. some animals have concurrent GI signs - can be very subtle.
How is a diagnosis of allergic skin disease made?
Eliminate other causes of pruritus, controlling infection, 6-8 week food trial. Allergy testing can be used to identify environmental allergens for avoidance or allergen specific immunotherapy.
What is acral lick dermatitis?
Chronic self trauma to the cranial and lateral aspects of the distal limbs. Most involve a long standing deep bacterial folliculitis, lichenification and scaring. numerous potential causes include behavioural problems, musculoskeletal problems, neurological disorders, pruritic skin disease. stress/anxiety can worsen allergic skin disease.
What are the signs of epitheliotrophic cutaneous T cell lymphoma?
Usually seen in older dogs, the clinical signs can be varied with diffuse or localised erythema, scaling, plaques, ulcers or nodules and pruritus.
What are the possible causes of alopecia in dogs?
Infectious - staphylococcal, demodex, dermatophytosis, leishmania
Immune mediated - dermatomyositis
Alopecia areata, vasculitis, vaccine associated vasculitis
Endocrine - hyperadrenocorticism, hypothyroidism, sex hormone dermatoses, telogen effluvium, paraneoplastic alopecia
Epitheliotrphic cutaneous t cell lymphoma
Congenital alopecias, follicular dyspnasias, cyclical flank alopecia, alopecia X
What are the clinical signs of Juvenile demodecosis?
Localised juvenile onset demodicosis occurs during adolescence and presents with multifocal alopecia, scaling, comedones and follicular casts. it isn’t pruritic unless there is a secondary bacterial or malassezia infection. Generalised demodicosis is more severe, more generalised alopecia, scaling, hyperpigmentation, comedones and follicular casts. Clinical signs may be limited to the feet. Secondary bacterial infection with papules, pustules, furunculosis and draining sinus tracts is common and may be life threatening. There is often peripheral lymphadenopathy with pyrexia and depression. The localised form usually resolves with maturity.
Why does adult onset demodicosis occur?
Usually secondary to an underlying disease e.g hyperadrenocorticism, hypothyroidism, diabetes, neoplasia etc. idiopathic cases also occr. the predisposition is probably inherited.
What is the treatment for demodex?
Amitraz dip once weekly. (toxic to chihuahuas and cats).
Lime sulphur dip safe and can be effective in mild cases.
Advocate spot on once weekly in milder cases.
Ivermectin or moxidectin - not licensed but can be used with care. (dont use in collies and related breeds MDR gene)
Milbemycin oxime once daily is effective and well tolerated even in MDR positive dogs.
How do you know when an animal has been succesfully treated for demodex?
Animals should be treated untill there are 2-3 negative skin scrapes at 7-14 day intervals and then for a further month.
What are the clinical signs of dermatophytosis in dogs and cats?
Multifocal alopecia and scaling. less common problems include paronychia, kerions, miliary dermatitis and fungal granulomas. Trichophyton species are more inflammatory causing alopecia, erythema, scaling, crusting and secondary bacterial infection.
What is the treatment for dermatophytosis?
Itraconazole licensed in cats.
Topical treatment on llocal lesions - chlorhexidine, enilconazole dip.
Environmental decontamination.
what are the clinical signs of leishmania?
Focal alopecia with a fine silvery white scaling, depigmentation, nodules, ulcer and crusting of the face, nose pinnae and feet. Lymphadenopathy, hepatomegaly, splenomegaly, anaemia, bleeding, ocular signs, kidney failure, lameness, muscle atrophy, pyrexia.
What are the dermatological changes seen with hyperadrenocorticism?
Bilaterally symmetrical truncal hair loss, comedones, atrophic and inelastic skin, prominent blood vessels and calcinosis cutis. Fragile skin and tearing is more common in cats.
What are the dermatological changes seen with hypothyroidism?
Truncal alopecia with thickened, hyperpigmented and cool skin (myxodema), partial alopecia with a faded coat.
What ar ethe igns of sertoli cell tumours?
Attraction to male dogs, gynectomastia, pendulous prepuce and linear preputial erythema.
What is feline paraneoplastic alopecia?
Associated with pancreatic and bile duct carcinomas. The cutaneous signs are highly specific and are usually noted before systemic illness. there is ventral truncal alopecia, with strikingly smooth, shining hthin and translucent skin, if diagnosed early enough the clinical signs are reversible with surgical excision of the tumour although metastases are common and prognosis generally poor.
What is cyclical flank alopecia?
Commonly causes seasonal hair los on the back and flanks in dogs, the underlying skin is darker but otherwise normal. hair loss and regrowth can vary from year to year. probably related to changes in day length.
What is aloopecia X?
Chows, pomeranians, keeshonds, poodles can suffer an unusual pattern of hair loss which starts in adolescence or young adulthood with loss of primary hairs, leaving wooly puppy like coat, eventually there is complete alopecia and hyperpigmentation sparing head and limbs.
What is miliary dermatitis?
An erythematous, papular and crusting dermatitis, commonly seen over the dorsal body, flanks, neck and head. Most commonly associate with flea allergic dermatitis
What is exfoliative dermatitis associated with in cats?
A rare paraneoplastic syndrome seen in older cats due to a thymoma with focal to generalised erythema, exfoliation and malassezia and or pyoderma.
What is lung digit syndrome?
Pulmonary tumours can metastasise to the digits, infiltrating P3 causing lung digit syndrome.
What is orofacial pain syndrome?
An uncommon problem - seen mostly in burmese and related cats, present with violent and frenzied self trauma of the mouth, face and neck, neurological problem - response to gabapentin/phenobarbital. Some cases have associated with herpes virus neuritis.
What are the symptoms of feline cowpox?
Resemble miliary dermatitis. Lesions are larger with a depressed centre that is usually covered with a small crust. careful examination will distinguish these from miliary lesions. Will also be a primary bite wound or scratch.
What is facial seborrhea?
Almost always seen in persian cats. affected cats present with thick, black greasy and tightly adherent scales overlying erosions around the eyes and nose. there may be secondary malassezia infection.
What is fragile skin syndrome?
an uncommon condition associated with cutaneous atrophy, tearing of the skin and poor wound healing. can be associated with hyperadrenocorticism and diabetes mellitus as well as long term steroid treatment.
How does ciclosporin work?(atopica)
It is an inhibitor of T cells. Inhibition of T cells and cytokine production has profound effects on various aspects of the immune system including antigen presentation, iGe production, mononuclear clel activity and development of inflammatory lesions. It also inhibits other cells in allergic reactions such as mast cells and eosinophils. Inhibition of T cell helper function and B cell activation could impair repsonse to vaccine - withdraw treatment for up to 2 weeks either side of vaccination.
What is hydrocortisone aceponate and why is this beneficial? (cortavance)
It is a topical non halogenated diester glucocorticoid. Esters at C17 and C21 ensure rapid absorption, potent anti inflammatory action and metabolism within the dermis into less active compounds, minimising cutaneous and systemic adverse effects.
How does oclacitinib work? (apoquel)
A targeted JAK1 inhibitor that specifically inhibits expression of IL-31 controlling pruritus in dogs with allergic dermatitis.
What are some primary causes of otitis?
Foreign bodies
Ear mites
Juvenile cellulitis
Atopic dermatitis/adverse food reactions
Other skin diseases - immune mediated, hormonal problems
allergic contact dermatitis (a whitish discharge with mature non degenerate neutrophils)
Ceruminous gland tumours - often obstruct ear canal and cause otitis before tumour is visible. most are benign.
Inflammatory polyps
Primary secretory otitis media - common in king charles spaniels.
What are the predisposing factors in otitis?
Conformation - pendulous, narrow, hairy ears
Warm humid climates
Over cleaning, wetting, traumatic cleaning, plucking hairs
Swimming - wetting and maceration o the ear canals (may also be a primary cause in some dogs especially in dirty, stagnant water which is often contaminated by pseudomonas)
Which products have synergistic activity against pseudomonas in the ear canal?
Polymixin B and miconazole.
Fluoroquinolones, gentamicin and polymixin B are usually effective against pseudomonas.
Which products have synergistic activity against staphs and streps in the ear canal?
Framycetin and fusidic acid
Which antibiotics are potentially ototoxic?
Ticarcillin, polymixin B, neomycin, tobramycin, amikacin
Which antibiotics could cause cartilage damage in young dogs
Fluoroquinolones.
What is necrotizing fasciitis?
A rare but severe form of cellulitis, rapid progression with severe cellulitis, swelling, necrosis, infection of deeper tissues, septicaemia and pyrexia.
What is sterile panniculitis?
Focal to multifocal painful nodules that ulcerate with fatty and bloody exdate.
What is puppy strangles?
Juvenile lymphangitis - causes acute onset pyrexia, lymphadenopathy, subcutaneous swelling and cutaneous exudation. Bacterial infection is uncommon and secondary despite the name. Treatment is usually based on 1-2 mg/kg prednisolone untill healed and then tapered. Prognosis is good if treated early and aggressively.
What bacteria may you pick up on skin cytology and what do these look like?
Staphylococci are large cocci that form diploid or irregular arrangements. Streptococci, micrococci and enterococci are smaller and form chains or irregular groups. Rod bacteria (bacilli) from the skin include pseudomonas, proteus and coliforms. Mycobacteria do not take up wright giemsa stains but pyogrannulomatous inflammation and the presence of small rod shaped vacuoles is suggestive.
What is the most common bacterial cause of skin infections in dogs?
Staphylococcus pseudintermedius
which antibiotics should be used in superficial pyoderma?
Clavulanate amoxicillin, clindamycin, cefadroxil, TMPS
Which antibiotics should be used in deep pyoderma?
cefovecin, clavulanate amoxicillin, pradofloxacin, cefadroxil
Which antibiotics are third line ?
Aminoglycosides, azithromycin, ceftazidime, chloramphenicol, clarithryomycin, florphenicol, imipenem, phosphomycin, piperacillin, rifampicin, tiamphenicol, ticarcillin.
What is hepatocutaneous syndrome?
A rare skin disease associated with end stage liver disease and pancreatic atrophy or glucagonomas. Clinical signs include erythematous plaques and erosions overlain by thick, yellowish adherent scales. Lesions usually occur at the mucocutaneous junctions, pressure points, ventrum, genitalia and feet with severe hyperkeratosis.
What are the clinical signs of zinc responsive dermatosis?
Common in arctic breeds probably hereditary. Clinical signs include bilaterally symmetrical scaling and alopecia of the face, pinnae, elbows, hocks, paws, genitalia and fissuring of footpads. the diagnosis is based on the history , clinical signs, biopsy and responsive to treatment.
What is pemphigus foliaceus?
Caused by auto antibody destruction of T cell membrane adhesion molecules resulting in loss of cohsion of superficial epidermal cells. triggers include bacterial and viral infections, chronic inflammatory dermatitis, drugs and neoplasia.
What is lethal acrodermatitis?
A rare hereditary condition of english bull terriers, causing stunted growth with scaling, crusting, erosions of extremities and pressure points, fissured footpads, onychodystrophy and concave hard palate. Por prognosis.
What are the symptoms of cutaneous lupus erythematosus?
commonly affects nasal planum causing loss of cobblestone appearance, swelling, depigmentation, erosions, ulcers and crusting.
What is seasonal nasal depigmentation?
Relatively common, benign disease with depigmentation of the nasal planum but preserving the cobblestone appearance with no erosion or crusting. May seasonally wax and wane.
What is ehlers danlos syndrome?
Abnormal elasticity of skin which may be fragile and tear easily. Also joint abnormalities and oseoarthritis.
What dose of glucocorticoids should be used to treat immune mediated skin disease?
Prednisolone 1-2mg/kg and 2-4mg/kg in cats
What diseases can ticks transmit?
Babesia, erhlichia, borrelia and bartonella.
How does infection with filamentous bacteria occur?
Infections with actinomyces and nocardia the filamentous bacteria are rare and usually inoculated by penetrating injury or foreign body. clinical signs include abscesses, ulceration and draining sinus tracts, panniculitis, nodules which may ulcerate and drain red brown to yellow grey fluid with tissue grains and systemic illness.
What does M lepraemurium cause in cats?what are the clinical signs?
Feline leprosy - causes multifocal crusting papules, erosions and granulomas, mainly head and forelimbs. A similar leproid granuloma syndrome is seen in dogs in the US.
What is onychorrhexis?
Splitting of the claws
What is onychomadesis?
Sloughing of claws
What is acanthosis nigricans? what breed are predisposed to this?
Seen in dachshunds and other breds that develop raised hyperpigmented plauqes, especially in the axillae and ventral abdomen. May be associated with malassezia and endocrinopathies.
which breeds tend to have the most and least aggressive mast cell tumours?
Boxers - less aggressive
Sharpeis - more high grade tumours at younger ages.
What is the best chemotherapy protocol for mast cell tumour metastasis?
Vinblastine, prednisolone and CCNU.
Which hormones does the anterior pituitary produce?
Adrenocortociotrophic hormone (ACTH) Thyroid stimulating hormone (TSH) Follicle stimulating hormone (FsH) Luteinising hormone (LH) Growth hormone (GH) Prolactin
What hormones does the posterior pituitary produce?
Oxytocin Atidiuiretic hormone (ADH)
What is pituitary dwarfism? how is this diagnosed?
A rare genetic disorder of GSD. defective development of pituitary gland leads to GH, TSH and prolactin deficiency and impaired release of FSH &LH. Puppies are skeletally stunted, retain soft wooly puppy coat, retain shrill puppy bark, retain deciduous teth and have fox like facial features, show cryptorchidism or anoestrus, show progressive lethargy and mental dullness.
What is feline acromegaly? what are the clinical signs?
Result of excess GH activity > results in soft tissue proliferation and insulin antagonism. usually due to a functional adenoma of the pituitary gland. It should be considered in any cat with diabetes mellitus which is resistant to insulin therapy. Clinical signs > polyphagia, polyuria, polydipsia, weight gain. Majority are male cats. Increased interdental spaces in the incisor teeth, Enlargement of the head, neck and paws - broad facial features, lion head, increased heart size, heart murmur, congestive cardiac failure, multiple limb lameness, increased size of the abdomen due to liver or kidney enlargement.
How can Acromegaly be definitively diagnosed?
Documenting grossly elevated serum IGf1 levels.
What is the cause of canine acromegaly & what are the clinical signs?
Progestagen excess, which induces GH production from the mammary gland. this occurs in intact bitches during dioestrus or due to exogenous progestagen administraion to suppress oestrus. it is not due to pituitary adenomas. Clinical signs are similar to cats except that DM is less consistent. neurological signs not a feature. History may reveal a recent oestrus cycle. panting and laryngeal stridor may occur due to soft tissue compression of upper airways.
What is the treatment for canine acromegaly?
Withdraw progestagen therapy, or ovariohysterectomy. if diabetic, insulin therapy.
What is the cause of central diabetes mellitus?
Failure in the normal synthesis and secretion of ADH by the pituitary gland. it can occur congenitally or as an acquired disease. in the latter case it may be due to trauma, inflammation or neoplastic damage to the pituitary gland. drugs may transiently cause DI eg adrenaline.
What is the cause of nephrogenic DI?
Results from a decreased responsiveness of th cells of the renal tubules and collecting ducts to ADH. rarely, this can be congenital. more commonly it is due to acquired damage to receptors in the renal cells by tubular necrosis, interstitial nephritis, pyelonephritis etc - hence secondary to some other underlying disease e.g hyperadrenocorticism, hyperthyroidism, hypercalcamemia, hypokalamemia, hepatic failure, pyometra, drugs including glucocorticoids.
how is diabetes insipidus diagnosed?
Normal haematology & serum bichemistry, hyposthenuria,
Assess unrestricted water intake and confirm as >100ml/kg.
Modified water deprivation and ADH response test. (time consuming, difficult to interpret, risk), an animal with PP will concentrate urine but if there is medullary washout,response may be minimal.
Can also just see response to AVP therapy - administer desmopresin into conjunctival sac. Dogs with Cdi will respond rapidly and those with NDI or PP will not.
How is CDI and NDI treated?
CDI - with DDAVP drops given intraocularly once or twice daily. Many owners opt to give only at night and allow dog free access outside during the day. If NDI is confirmed then search for underlying cause and treat this. if none is find, found, feed a low salt diet and give chlorthiazide diuretics.
What is the cause of primary hypothyroidism in dogs?
Lymphocytic thyroiditis and idiopathic follicular atrpohy. Lymphocytic thyroiditis is an immune mediated disorder which results in progressive destruction of the thyroid gland by infiltrating lymphocytes, plasma cells and macrophages. In idiopathic follicular atrophy there is a loss of thyroid parenchyma and replacement by adipose connective tissue. Thyroid neoplasia resulting in destruction of thyroid tissue is an uncommon cause of hypothyroidism in dogs.
What are the clinical features seen with dogs who have hypothyroidism?
Mean diagnosis 7 years.
General insidious in onset clinical signs. Lethargy, weight gain, exercise intolerance and cold intolerance. Alopecia, bilaterally symmetrical or patchy, thinning of hair on tail, skin may also bruise more easily and have poor wound healing, may fail to regrow hair following clipping, myxoedema is a non pitting thickening of the skin particularly eyelids, cheeks and forehead. Irregular oestrus cycles and anoestrus. Sinus bradycardia and weak apex beat. Reduced ventricular function may occur in hypothyroidism. Ocular changes associated with hypothyroidism include corneal lipidosis, uveitis and keratoconjunctivitis sicca.
What blood changes are seen in hypothyroidism?
A mild non regenerative anaemia occurs in 30% of hypothyroid dogs. Fasting hypercholesterolaemia and hypertriglyceridaemia occurs in around 75% of dogs with hypothyroidism.
How is hypothyroidism diagnosed?
Total T4 - a normal T2 concentration demonstrates that a dog is euthyroid (UNLESS anti t4 antibodies cause an increase in T4 concentration) . A low T4 does not confirm a diagnosis of hypothyroidism. decreased T4 may also occur due to a non thyroidal illness. Measurement of Free T4 does not always remain within referance range in dogs with sick euthyroid syndrome, but should give a more accurate measurement of thyroid function since only free hormone can enter cells.
In primary hypothyroidism, negative feedback should result in TSH concentrations increasing above the reference range. Many dogs with hypothyroidism have a TSH concentration within the reference range.
thyrotropin (TSH) stimulation test - measure of T4 before and after TSH administration is a test of thyroid function reserve - most accurate test for diagnosis. Dogs with primary hypothyroidism will not have a significant increase in TT4 post TSH stimulation.
What is the treatment of choice for Hypothyroidism?
Synthetic l thyroxine (t4). (soloxine, thyroxyl). A liquid formulation (leventa) is also available. initial dose of 0.02-0.04 mg/kg once dail or divided as twice daily dose is recommended.
what is the cause of hyperthyroidism?
In the majority of cases it is caused by a functional adenoma, which may be unilateral or bilateral. 2% of cases are due to thyroid neoplasia.
What are the clinical signs of hyperthyroidism?
Older cats
Weight loss, polyphagia, polyuria, polydipsia, intermittent vomiting and diarrhoea, altered behaviour including irritability/aggression, lack of or excessive grooming. Poor body condition, palpable goitre, tachycardia, gallop rhthmn, cardiac murmur, tachypnoea, plantigrade stance or cervical ventroflexion from mscle weakness, matter unkempt coat or alopecia. Systolic blood pressure may be elevated due to increased sympathetic output.
How is a diagnosis of hyperthyroidism made?
Elevated T4: this is most commonly performed, but concurrent illness may lower thyroxine into the upper half - normal range in the hyperthyroid cat. Tsh is suppressed in hyperthyroidism.
What are the management options for hyperthyroidism in cats?
Medical management - inhibit the enzyme thyroid peroxidase which is involved in a number of steps in the formation of T4 and T3. E.g Methimazole - twice daily dosing. (side effects include facial pruritus, hepatopathy, aplastic anaemia, vomiting, dx)
Carbimazole - metabolised into methimazole. Sustained release product vidalta is licensed for once daily dosing.
Dietary management - Severely restricting dietary iodine, then the thyroid glands is unable to synthesis thyroxine and t3. only fed EXCLUSIVELY on this diet.
Radioactive iodine - best therapy - recurernce is rare. Typically administered by subcut injection, cat held in isolation.
Surgical management - ideally should be stabilised prior to surgery. Can offer cost effective treatment, recurrence is likely in 1/5 of patients even where bilaterally thyroidectomy is performed due to ectopic thyroid tissue.
What are the common causes of hypercalcaemia?
Malignancy - lymphoma, anal sac adenocarcinoma, multiple myeloma, carcinomas, malignant melanoma, osteosarcoma, thymoma. Hypoadrenocorticism Chronic renal failure Primary hyperparathyroidism Hypervitaminosis D Granulomatous disease Idiopathic (cats) Young animals
What is primary hyperparathyroidism?
Most commonly associated with a solitary adenoma of the parathyroid gland resulting in atrophy of the other glands. the tumour does not respond to usual feedback control so high PTH secretion continues despite high calcium concentrations.
What breed are predisposed to primary hyperparathyroidism?
Keeshond
What are the clinical signs of hypercalcaemia?
PUPD, listessness, weakness, exercise intolerance, inappetance, muscle wasting, urinary tract signs such as dysuria, haematuria due to urinary tract infection or uroliths, vomiting, constipation, shivering, stiff gait.
How is primary hyperparathyroidism diagnosed?
by the finding of persistently increased calcium concentrations in the presence of an inappropriately increased Plasma PTH cocentration. Serum phosphate concenrations tend to be below the referance range or normal which means that the risk of soft tissue mineralisation is low. Most parathyroid adenomas can be detected by ultrasound by experienced ultrasonographers.
What is the treatment/management of primary hyperparathyroidism?
IV fluid therapy 2-3 times maintenance 0.9% NaCl is advisable in patients with symptomatic hypercalcaemia pending a definitive diagnosis. Surgical removal of parathyroid mass id avisable in al symptomatic cases. The hypercalcaemia typically resolves between 1-3 days post surgery.
How does secondary hyperparathyroidism occur with chronic renal failure?
Progressive renal disease reduces excretion of phosphorous resulting in hyperphosphataemia and a reciprocal reduction in serum calcium. > an increase in PTH secretion.Typically dogs and cats with CRF will either have normal or low total calcium and only a small minority develop hypercalcaemia. The clinical signs may be related to renal disease or associated with prolonged PTH secretion - may have rubber jaw, bone pain, pathological fractures.
What is nutritional secondary hyperparathyroidism?
a nutritional disorder that occurs in puppies and kittens that have been fed diets that contain an excessive amount of phosphate and insufficient calcium.Usually all meat diets. Lack of dietary calcium leads to increased PTH concentrations. > calcium resorption from bone > lameness, reluctance to stand or walk and skeletal pain.
What diseases can cause hypocalcaemia in dogs and cats?
Primary hypoparathyroidism Eclampsia Acute pancreatitis Hypoalbuminaemia Acute or chronic renal failure Nutritional secondary hyperparathyroidism Protein losing enteropathies Ethylene glycol toxicity
What is primary hypoparathyroidism?
A rare condition which occurs following immune mediated destruction of the parathyroid glands. (also during damage when removin thyroid in hyperthyroid cats). Absence of PTH production leads to a decrease in plasma calcium concentration and an increase in phosphate concentration.
What are the clinical signs of hypoparathyroidism?
Female predisposition - commonly affets poodles, min schauers, retrievers, gsd. typically age of onset is 5yo. Clinical signs tend to be related to sudden onset of neuromuscular or neurological disturbances which may be worsened or initiated by exercise or excitement. These include nervousness, behavioural changes, focal muscle twitching, muscle cramps, stiff gait, pyrexia, tetany and seizures.
When should primary hypoparathyroidism be suspected?
In a dog or cat with persistent hypocalcaemia, hyperphospataemia and normal renal function. Diagnosis is confirmed by identifying low plasma PTH concentration with concurrent hypocalcaemia.
What is the treatment for primary hypoparathyroidism?
Administration of vitamin D and calcium supplements which is typically divided into acute and chronic treatment phases. in acute - administration of calcium gluconate until clinical signs are controlled. Once stable - oral treatment with vitamin D and calcium supplementation.
Which zones of the adrenal gland produce which hormones?
Cortex produces - aldosterone form the zona glomerulosa, cortisol from the zona fasciculata and zona reticularis, and sex hormones from the zona reticularis. All are synthesised from cholesterol.
the medulla secretes catcholamines adrenaline and noradenaline from chromaffin cells.
What are the effects of aldosterone?
Increased sodium resorption, increased renal excretion of potassium, increased water resorption.
What is the usual cause of canine hyperadrenocorticism?
A pituitary neoplasm causing autonomous excessive ACTH secretion in 85-90% of cases. Adrenal dependent HAC is due to adrenocortical neoplasia.
What are the clinical signs of hyperadrenocorticism?
Polyphagia PUPD Pendulous or enlarged abdomen/obesity Hepatomegaly Excessive panting Muscle atrophy Lethargy skin changes - hyperpigmented, infection, seborrhea, poor wound healing, thin skin Alopecia - bilaterally symmetrical, non pruritic, dull dry coat Anoestrus/testicular atrophy Calcinosis cutis Hypertensive retinopathy
What biochemical abnormalities are associated with hyperadrenocorticism?
Raised AP Bile acid concentrations may be normal or marginally elevated Hypercholesterolaemia Hypertriglyceridaemia High normal glucose Low thyroxine in 70% of cases.
How is Hyperadrenocorticism diagnosed?
Basal cortisol secretion - fluctates and so basal cortisol should not be used for diagnosis.
ACTH stimulation test - investigates capacity of adrenal cortex to produce cortisol. The enlarged adrenal cortex in HAC response to ACTH with excessive cortisol production.
Low dose dexamethasone suppression test - Doses of exogenous glucocorticoids suppress blood cortisol concentrations of healthy dogs by negative feedback but are less effective in dogs with naturally occurring HAC. Most dogs with ADH do not suppress at either point, whereas those with PDH may suppress at 4 ours but not at 8 hours.
Urinary cortisol/creatinine ratio - cortisol is excreted in urine so ratio provides reliable estimate of cortisol release.
How can you differentiate PDH ADH and iatrogenic HAC?
Imaging - in PDH both glands are enlarged. In ADH one gland is enlarged and the other is atrophied.
Low dose dexamethasone test - 30% of dogs with PDH suppress cotisol at 4 hours but not 8 hours. Dogs with iatrogenic HAC have atrophic glands of ultrasound imaging.
What is the treatment for Pituitary dependent hyperadrenocorticism?
trilostaine - competitive and reversible inhibitor of 3B hydroxysteroid dehydrogenase so blocks adrenal steroid biosynthesis pathway.
Mitotane - cutotoxic and destroys the zona fasciculata and reticularis of the adrenal gland while leaving zona glomerulosa mostly intact. only permitted if trilostane fails to control condition.
What is the treatment for adrenal dependent hyperadrenocorticism?
surgical removal of adrenal tumour. Trilostane has been reported to be effective in managing adrenal tumours Mitotane is relativelye ffective in adrenocortical neoplasia as it is cytotoxic.
What is the typical presentation of hyperadrenocorticism in cats?
Diabetes mellitus. Cats with insulin resistant diabetes mellitus should always be assessed for presence of HAC.
Extreme skin fragility. skin will tear easily even with normal handling and large areas may denude.
Weight loss - due to poorly controlled diabetes.
What is the cause of canine hypoadrenocorticism?
Primary HOC usually arises from idiopathic bilateral adrenocortical atrophy which is thought to be an immune mediated process.
What ar ethe typical clinical signs of hypoadrenocorticism?
75% of cases are female Young to middle aged dogs (median 4yo) Inappetance Depression Weakness Vomiting Diarrhoea Weight loss shivering, muscle tremors, stiffness PUPD Collapse Dehydration Hypotension Bradycardia and weak pulse Muscle weakness Mild normocytic normochromic anaemia
What are the biochemical features seen with hypoadrenocorticism?
Hyperkalaemia
Hyponatraemia
Hypochloraemia
Reduced plasma:sodium ratio. (
