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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;
1. stiffness after rest
2. pain in atleast one joint
3. swelling of at least one joint
4. swelling of atleast one other joint in 3 months
5. symmetrical joint swelling
6. subcutaneous nodules
7. erosive lesions on radiography
8. positive rheumatoid factor
9. poor synovial fluid mucin clot
10. characteristic synovial histopathology
11. 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?



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


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?



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
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?



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



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)


What hormones does the posterior pituitary produce?

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.
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?



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
Acute pancreatitis
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?

Pendulous or enlarged abdomen/obesity
Excessive panting
Muscle atrophy
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
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)
Weight loss
shivering, muscle tremors, stiffness
Bradycardia and weak pulse
Muscle weakness
Mild normocytic normochromic anaemia


What are the biochemical features seen with hypoadrenocorticism?

Reduced plasma:sodium ratio. (


What changes are seen on electrocardiography with hypoadrenocorticism?

Spiking of the T wave
Shortening of Q-t interval
Prolonged P-r interval
Reduced P wave amplitude
P waves may disappear. Severe bradycardia, ventricular fibrillation and cardiac arrest may result.


How is hypoadrenocorticism diagnosed?

A basal cortisol level


What management is needed in acute primary HOC?

Appropriate fluid therapy - isotonic salive IV, which raises sodium levels and reduces potassium levels and corrects hypovolaemia.
If hypoglycaemic - dextrose may be added to fluids.
Give glucocorticoids immediatley after the ACTH stimulation test has been completed. Drug of choice is hydrocortisone sodium succinate administered IV.
Monitor sodium and potassium concentrations hourly.


what is maintenance therapy for HOC?

Oral mineralocorticoid therapy using fludrocortisone acetate. Some will respond well to daily dose of prednisolone as well even when serum electrolytes are normally. Glucocorticoid dosage should be initiated/increased in times of stress.


What is atypical hypoadrenocorticism?

Typical clinical and pathological features of glucocorticoid insufficiency but normal serum electrolyte concentrations and no clinical signs related to these - subnormal response in ACTH test. May just have early HOC - should receive physiological replacement of glucocorticoids and be monitored carefully for development of mineralocorticoid deficiency.


What is conns like syndrome?

Feline primary hyperaldosteronism. Uncommon. Autonomous excessive secretion of aldosterone> excessive sodium retention > excessive potassium secretion. usually due to a unilateral adrenal tumour. Causes hypokalaemia which can be mild and episodic, hypertension (retinopathy, intraocular haemorrhage, acute onset blindness). Consider in cases of severe hypertension where hypokalaemia responds poorly to potassium supplementation. There is an elevated plasma aldosterone with concurrent low plasma renin levels.


what is a phaeochromocytoma? what are the clinical signs?

functional tumours of the chromaffin cells of the adrenal medulla. usually unilateral. they cause excessive production of catecholamines. release is episodic so clinical signs are intermittent; weakness and lethargy, episodic collapse, restless, panting, anxious, tachycardia, hypertension, pupd. Local invasion common, particularly the caudal vena cava where tumour thrombus may form.


How does radioactive iodine treat hyperthyroidism?

I131 is selectively taken up by the thyroid to be incorporated into thyroid hormone precursors. it emits beta and gamma radiation and so destroys the thyroid tissue. it is selective and not associated with damage to surrounding tissue e.g parathyroid. the draw backs include special facilities and hospitalisation of the cat post treatment as the i131 is eliminated in faeces, urine etc.


Which type of diabetes mellitus is most common in dogs and cats?

type 1 in dog
Type 2 in cats


How do oral hypoglycaemic agents the sulphonylurea derivatives work?

They stimualte the pancreas to release insulin and increase the peripheral utilisation of insulin. glipizide is the main agent used. It inhibits ATPH-dependent K+ channels causing depolarisation and release of insulin. Kinetics based on human studies show good oral bioavailability with hepatic metabolism and renal excretion.


What are Microsomal triglyceride transport protein inhibitors?

Used for obesity. MTP and apolipoprotein B are key lipid transfer proteins. Required for the formation of apoB containing lipoproteins, this occurs in enterocytes and the liver within the endoplasmic reticulum. Inhibition of MTPs results in lowering of cholesterol and triglyceride levels , and reduction in absorption of dietary fat and increased faecal excretion of fat.


What do alpha cells of the pancreas secrete?



What do beta cells of the pancreas secrete?



Which insulin is feline insulin most closely related to?



Which insulin is canine most closely related to?

Porcine - they are identical


What is type 1 diabetes mellitus?

Insulin deficiency diabetes associated with a total loss of beta cell function. Common in dos. High blod glucose, low resting insulin, fail to secrete insulin in presence of hyperglycaemia. insulin dependent.


What is type 2 diabetes mellitus?

Insulin resistance diabetes. Patients have high resting blood glucose, normal/high levels of insulin > insufficient for demand. most occur because of insulin resistance due to excess diabetogenic hormones or obesity. Peripheral cell insulin receptors are less responsive to insulin, meaning ever hgiher insulin levels are acquired.


What are the predisposing factors to diabetes?

Progesterone (entire females) > production of growth hormone > diabetogenic.
Glucocorticoids - antagonise insulin

Pancreatitis - chronic pancreatitis may lead to sufficient loss of endocrine tissue to result in DM.


What is the renal threshold for glucose?

10-12mmol/l in dogs and 12-14mmol/l in cats.


What are the clinical signs of Diabetes mellitus?

Polpyhagia, PUPD.
If ketoacidotic - depression, anorexia, vomiting, dehydration
Cats may exhibit a plantigrade stance due to peripheral neuropathy


How is diagnosis of DM made?

Clinical signs
Persistent fasting blood glucose greater than 14mmol with glucosuria. hyperglycaemia can be as high as 35mmol/l. In cats hyperglycaemia can occur due to stress up to 16mmol/l. Measurement of fructosamine levels may help with interpretation of moderately high blood glucose


What is fructosamine?

Produced by the irreversible glycosylation of albumin in proportion to surrounding glucose levels. its half life is around 1-2 weeks and so levels give an indication of the average blood glucose level over that time span.


What are the complications of poorly controlled dM?

Formation of cataracts in dogs
Retinopathy (rare)
peripheral neuropathy in cats
Recurrent bacterial infections - uti,skin, dental
life threatening diabetic ketoacidosis.


What are the possible differentials for hypoglycaemia?

hunting dog, toy dog or neonatal hypoglycaemia
Prolonged starvation
Glycogen storage disease
hepatic insufficiency
toxins (ethylene glycol, xylitool)
extrahepatic IGF-2 producing tumours


What is a gastrinoma? what are the clinical signs?

Gastrin secreting tumour in the pancreas. the clinical signs relate to overproduction of gastric acid, with vomiting, anorexia, diarrhoea, gastroduodenal and oesophageal ulceration and perforation, haemtemesis.


How thick is enamel in cats and dogs?

0.2mm in cats and 0.5mm in dogs


What is the periodontal space?

This is the narrow space that exists between the tooth and the alveolar bone of the jaw in which the tooth is situated. the periodontal space contains the periodontal ligament, blood vessels, nerves and lymphatics.


What are sharpeys fibres?

Fibres of the periodontal ligament which unite the alveolar bone on one side and the cementum on the other in a meshwork of inter woven branches.


How deep should the gingival sulcus be?

up to 1mm in cats and up to 4mm deep in dogs. deeper pockets indicate tooth disease and attachment loss.


Which blood vessels supply the mandibular teeth?

The mandibular artery enters the mandible at the manidbular foramen and becomes the inferior alveolar artery. it runs within the mandibular canal and exits at the mental foraminae where branches are now called the mental arteries. along the way, small branches supply individual teeth by penetrating the periodontium.


Which blood vessels supply the maxillary teeth?

The maxillary artery and its branches supply these teeth. The main branch running within the infraorbital canal, is the infraorbital artery.


What is the dental formula of a dog? (primary and permanent)

Deciduous teeth - I 3/3 C 1/1 PM 3/3 M 0/0-28 teeth in total

Permanent teeth - I 3/3 C 1/1 PM 4/4 M 2/3 - 42 teeth in total


What is the dental formula of a cat? (deciduous and permanent teeth?)

Deciduous I 3/3 C 1/1 PM 3/2 M 0/0
Permanent I 3/3 C 1/1 PM 3/2 M 1/1


When should puppies/kittens teeth erupt?

No teeth at birth
Deciduous canines by 4 weeks
Incisors, premolars through by 5-6 weeks.
All deciduous teeth present and correct by 6 weeks in both kittens and puppies.

Permanent teeth
Incisors, canines - 3 months
Premolars - 4 months
Molars - 5 months

So a puppy or kitten should have all of its primary teeth at 1st vaccination and may be beginning to show early secondary incisor and canine eruption at 2nd vaccination.


What is the basic mechanism of periodontal disease?

Supra gingival and sub gingival plaque accumulates > bacteria colonise. Initial bacteria are aerobes and facultative anaerobes. As condition progresses > oxygen levels in gingival sulcus reduce > anaerobes take over > periodontal pockets form due to tissue destructive actions of bacterial toxic by products.

Normal gingiva > plaque > inflamed gingival margin > fluid accumulates in gingival sulcus >bacteria colonise > cellular infiltrate develops > junctional epithelium swells > tissue destruction at periodontal ligament and alveolar bone crest begins > pocket deepens and widens > debris accumulates in pocket > bone resorption progresses > toth becomes progressively more mobile. > eventually lost.


Which suture material should you use to suture a canine gingival flap you have made?

Monocryl 4/0 or 5/0


What are feline odontoclastic resoprtive lesions?

the initial lesions is an external surface resorption of teh tooth root by multinucleate cells called odontoclasts. hard tissue loss starts in the root cementum, progresses into dentine and then moves up into the dentine of the crown. Eventually the enamel is also eaten away in a scalloped fashion giving the characteristic clinical lesion of a shiny bright red area on the crown surface. the red substance is a granulation like tissue filling in the enamel void.


Which teeth are most commonly affected with FORLS?

The lesions are almost always located on the buccal aspect of the tooth and certain teeth are more commonly affected. The mandibular third premolars on the LHS 307 and 407 on the RHs are often the first affected. Many of the cats with broken or missing teeth that you see in practice will have had this condition.


What are the clinical signs of FORLS in cats?

Painful, irritability, changes in food preferance, drooling, head shyness.


What is a type 1 FORL lesion?

Normal tooth root density and appearance, periodontal ligament space visible, often associated with general periodontal disease.


What is a type 2 FORL lesion?

Roots hard to see, may be replaced by alveolar bone or ghosted in outline, the periodontal ligament space is not clear, gingivitis associated with the affected tooth rather than general periodontal disease.


What is the treatment of FORLs?

Teeth affected by crown enamel resorption should almost always be extracted. Type 1 lesions require standard extraction with root retrieval. If a root tip fractures it should be found and removed. Type 2 lesions can be treated with coronal amputation. the crown is amputated and no attempt is made to retrieve roots. the flap can be replaced using a suture with monocryl.


What is feline chronic gingivo stomatitis?

The aetiology is uncertain but the condition appears to be an aberrant immune response to low levels of plaque antigens. Associations are suggested with feline calicivirus, FeLV, FIV and FHV, Increased numbers of cats in the household or social stress, gram negative anaerobes, purebreeds. The lesion is a submucosal infiltration of plasma cells, lymphocyts, macrophages and neutrophils. the palatoglossal folds and the oral mucosa lying lateral to these are most commin sites for inflammation.


What is the treatment for feline chronic gingivo stomatitis?

Supply a 10 day course of antibiotic. suitable choices are clindamycin, metronidazole, amoxicillin clavulanate. then perform a careful scale and polish including subgingival treatment, extract teeth affected by periodontal disease and FORLS. supply chlorhexidine based gel for the owner to apply daily on an on going basis. Unfortunately many cases will persist after the above treatment. Other possibilities include, removal of all cheek teeth, upper and lower quadrants, both sides.Radical extraction results in improvement in 87% of cases. Steroids may be a good option for the owner if unable to afford extensive treatment. Interferon can be used for cats non responsive to radical extractions. The interferon is given sub gingivally or subcut until the cat tests FCV negative.


A 2-year old MN DSH presents for anorexia and vomiting of 2 days duration. Physical examination reveals the cat is dehydrated, but otherwise no abnormalities are noted.

Bloodwork shows the following: BUN 55 mg/dl (19-34 mg/dl), creatinine 3.8 mg/dl (0.9-2.2 mg/dl), sodium 135 mEq/L (146-156 mEq/L), potassium 3.1 mEq/L (3.7-6.1 mEq/L), chloride 85 mEq/L (115-130 mEq/L), TCO2 38 (13-21 mEq/L), HCT 60% (30-45 %). Urinalysis: USG 1.058 (>1.035), negative sediment.

You started the cat on 0.9% NaCl IV to treat the dehydration. Based on this history and blood results, what is your top differential diagnosis?

Because of this cat's history and blood results, an upper GI obstruction is highly suspected. Hypochloremic metabolic alkalosis is a classic finding in a pet with an upper GI obstruction and should be ruled out first, especially in a young cat with these clinical signs.


How is feline panleucopaenia virus transmitted?

Faecal oral route , by direct contact and via environmental contamination. very sable and can survive for over a year at room temperature in organic material.


What are the symptoms of feline panleucopaenia virus?

In utero - death resorption or abortion.
In late stage of gestation - kittens with profound and permanent suppression of immune system (lymphopenia and neutropenia).
Infections in older kittens - typically follow incubation period of up to 10 days and rage from subclinical to peracute death. Mild forms include self limiting diarrhoea and panleucopaenia. Other kittens may show profound diarrhoea, secondary bacterial infection, panleucopaenia, sepsis and death. Affected kittens often present with a sudden onset of depression, anorexia, pyrexia and apparent thirst but do not actually drink. vomiting and diarrhoea, may contain blood, marked dehydration and collapse.


How is diagnosis of feline panleucopaenia virus made?

Presence of clinical signs, vaccinal status, age, and environment, accompanied by profound panleucopaenia, particularly neutropaenia. Virus isolation or PCR tests can be performed on faecal samples, oropharyngeal swabs in transport media or post mortem material. Canine parvo snap tests can be used for detection of antigen in faeces.


What is the treatment of feline panleucopaenia?

Supportive care - fluid therapy, broad spectrum antibiotics, anti emetics, gut protectants, B vitamins, provision of a warm clean environment, good nursing care, feline interferon omega can be very helpful.


What is the cause of cat flu?

over 80% of cases are caused by infection with either feline calicivirus or feline herpes virus. Other oragnisms may be involved including feline coronavirus, mixed bacteria, bordetella bronchiseptica, pasteurella multocida and mycoplasma and chlamydophila felis.


How is cat flu spread?

Most of the organisms that typically cause cat flu are transmitted by aerosol and direct contact of the eyes, noses and mouths.


What does feline calicivirus cause?

Ulceration of the tongue, hard palate, soft palate, pharynx and external nares.


What are the clinical signs of cat flu?

Sneezing is typically the first sign observed, followed by a serous ocular and nasal discharge which rapidly becomes mucopurulent due to secondary bacterial infection. Affected cats are usually depressed and pyrexic. conjunctivitis can cause the eyelids to become sticky. coughing and dyspnoea are less commonly seen and tend to be associated with FHV and B bronchiseptica.


How should diagnosis of cat flu be confirmed?

presumptive diagnosis made on clinical signs and history of possible exposure to causal organisms. Nasal or oropharyngeal swabs can be taken for isolation and culture and in the case of FHV1 and C felis, PCR tests. Serology can be used to determine whether or not a cat has been previously exposed to FCV or FHV - limited value since most cats have been vaccinated.


What is the treatment for cat flu?

symptomatic therapies and good nursing care.
Feline IFN omega may be helpful as an antiviral. Other options are oral famcyclovir ororal L lysine. Safeb road spectrum antibiotics for 2-3 weeks. Where B bronchiseptica, mycoplasma or C felis have been detected give doxycyline. Oesophageal feeding tubes are preferred as the cats nasal turbinates are already inflamed. Mirtazapine can be used as an appetite stimulant Mucolytics may help to ease respiratory tract congestion e.g bromhexine (bisolvon)


What is the causal organism of feline infectious anaemia?

Mycoplasma haemofelis, M turicensis and mycoplasma haemominutum.


What does FIA cause?

The parasites adhere to red blood cells changing their cell surface and making them antigenic so they are removed by the spleen and liver. the replication cycle of this parasite takes 2-8 weeks so clinical disease tends to be cyclic. Infection may be subclinical but most likely to result in disease when the cat is co infected with FelV.


How is feline infectious anaemia spread?

Via saliva through biting and possibly fleas. Transmission from queens to kitens in utero or via milk may also occur.


What are the clinical signs of feline infectious anaemia?

May be asymptomatic or just show fever. other cats develop acute disease with signs of lethargy, pale mm, tachypnoea, tachycardia and occasionally dyspnoea. splenomegaly is common and pyrexia is variable. Where the anaemia is severe a haemic murmur may be detected.


How can FIA be diagnosed?

Parasitaemia waxes and wanes, but giemsa or acridine orange stained blood smears can be used for detection of the organism attached to red cells. Detection of the organism is variable and repeat smears may be required. A regenerative anaemia should be present, with polychromasia and normoblasts.


What is the treatment for feline infectious anaemia? (Mycoplasma haemofelis)

Doxycyline 5-10mg/kg/day PO. where AIHA is present give prednisolone.


Which FELV antigen is detected in the FELV test?

P27 - it is the most abundant of the core proteins.


How is FelV spread?

Transmitted by cat to cat contact, with the virus being excreted in saliva, biting, licking and mutual grooming are important means of virus transfer, urine, faeces and milk.


How do cats with latent FELV infections test?

Infection is maintained in bone marrow, inadequate virus is present to result in a viraemia so these cats are usually negative on conventional FeLV elisa and IFA tests. In latent infections the virus can sometimes be identified on bone marrow samples by culture or PCR.


What are/ the Diseases related to FeLV infection

Immunosuppression - causing cytopenia, neutrophil and lymphocyte dysfunction and thymic atrophy. May predispose to opportunist infections.
Anaemia - Regenerative anaemia due to FELV associated immune mediated haemolytic anaemia or due to M haemofelis infection wihlst marrow disorders can result in non regenerative nanaemia. Pure red cell aplasia can result form felv subgroup C infection.

Neoplastic diseases - lymphoma is the most common type. Can be multicentric or disseminated. The multicentric form is seen as LSA affecting several separate sites such as the kidneys, nose and nervous system.

Myeloproliferative disorders can result from FeLV infection where proliferation of a myeloid cell ine in a myeloid leukaemia can result in crowding out of other non malignant marrow cell lines.

Felv can also cause severe haemorrhagic enteritis, similar to FPV infection.


What sort of virus is FIV?

A lentivirus


What type of cat is most likely to be infected with FIV?

Older male cat that is free to roam outdoors. The major route of transmission is via saliva, especially through biting so those cats exhibiting territorial aggression are most at risk.


Describe the pathogenesis of FIV?

primary phase - virus replicates rapidly in lymphoid tissue. 3 weeks after infection. may be subclinical. More typically it results in pyrexia, malaise, lymphadenopathy. Most cats then become asymptomatic and remain healthy for an indefinite period of time. during the asymptomatic phase, levels of ciruclating virus are low but viral replication continues within infected tissues. Immunosuppression develops as the virus causes a reduction in CD4+ T helper cell numbers. Both cell mediated immunity and humeral immunity become defective as T and B lymphocyte function is suppressed. initial signs are usually secondary infections.


What are the clinical signs of infection with FIV?

Gingivitis/stomatitis, weight loss, rhinitis, diarrhoea, skin disease and ocular signs. Fever, lymphadenopathy, respiratory disease, otitis, recurrent abscesses, chronic enteritis, chronic renal insufficiency. Many infections to which healthy cats would usually show greater resistance - eg demodicosis, dermatophytosis, toxoplasmosis. Incidence of neoplasia is also increased - lymphoma, myeloproliferative disease, squamous cell carcinoma, mammary gland carcinoma.Clinical signs are v similar to those associated with FeLV.


How is FIV definitively diagnosed?

By detecting either virus or FIV specific antibodies in blood or saliva. Elisa CITE and Snap tests detect antibodies to core protein FIV P24, while RIM tests detect antibodies to envelope protein gp40.


you have a cat that has tested positive for FIV and has dermatophytosis - what should you treat it with?

Itraconazole rather than griseofulvin since griseofulvin can induce severe neutropaenia in cats.


What is the causal agent of Feline infectious peritonitis?

Feine coronavirus. Up to 40% of the general population have antibodies against FCOV, many are usually harmless and at most cause only mild enteric signs, however it is believed that when FCOVs are able to replicate rapidly they undergo mutation and this can lead to increased pathogenicity. This enables the viruses to infect macrophages and in some cases cause FIP.


How is FCOV transmitted?

Faeco - oral route. higher incidence of FIP in cats housed in colonies and burmese, persian birman and bengal breeds.


What are the clinical signs of FIP?

Effusive / wet form - fluid accumulates in peritoneal and/pleural cavities with lesions on peritoneum and pleura.
Non effusive/dry form - small focal lesions develop in the peritoneum, kidneys liver mesenteric LN and pancreas.
The eyes are often involved presenting as anterior uveitis and posterior uveitis.

the history usually includes anorexia, weight loss, pyrexia, dullness.


Describe the life cycle of toxoplasma gondi?

Definitive host - cat, oocysts are passed in faeces, ingested by intermediate host (mouse/rat),, then cats usually become infected by ingestion of encysted organisms present in the tissues of a chronically infected intermediate host. the cyst wall is digested by the cat,, releasing infectious organisms which penetrate the intestinal wall and replicate throughout the body as rapidly dividing tachyzoites. The organisms invade and replicate in the intestinal epithelial cells where sexual reproduction results in the formation of oocysts which are excreted in the faeces.


When are toxo oocysts shed in cat faeces?

Cats previously unexposed to T gondii usually begin shedding oocysts between 3 and 10 days after ingestion of ingested tissue, and continue shedding for around 10-14 days, during which time many millions of oocysts may be produced. Once immune, further shedding of oocysts is extremely rare. After oocysts have been passed in the faeces they undergo sporulation which takes 1-5 days. Prior to this they are not infectious. Oocysts are very resistant and may survive in the environment for well over a year.


How do intermediate hosts of toxo become infected?

Rodents, birds, sheep, pig, cattle, become infected by ingestion of sporulated oocysts. An extra intestinal cycle of infectious occurs and results in encysted bradyzoites which are infectious to cats and other intermediate hosts.


What are the clinical signs of feline toxoplasmosis infection?

Clinical disease v rare. most common in young cats, may be due to a poorly developed immune response. Reactivation of infection in older cats linked to co infection with FIV or FELV. most common clinical signs are anorexia, weight loss, lethargy, dyspnoea due to pneumonia, ocular signs, iritis, chorioretinis and pyrexia.


How is toxplasma diagnosed?

Looking for faecal oocysts > clinical signs do not usually develop untill after oocyst shedding has caesed.
Serology - igG seroconversion occurs after 2-4 weeks with peak titres by 4-6 weeks. However in many cases clinical signs will develop either before seroconversion occurs or not untill after peak titres have developed. IgG serology is therefore often difficult to interpret and a single antibody titre is rarely of any value. High Igm titres demonstrate recent or reactivated infection with T gondi.


What is the treatment of choice for feline toxoplasma.

Azithromycin good second choice.


Does owning a cat increase the risk of acquiring toxoplasmosis?

No - infection is correlated with eating undercooked meat.


How do cats become infected with cowpox?

Cats are usually infected with cow pox by bank voles, field voles and wood mice which are known to carry the infection. It can also be occasionally found in the house mouse. Affected rodents do not usually show signs of infection.


What are the clinical signs of cowpox?

The virus enters the skin through a bite wound, infection becomes apparent after a few days as a small ulcerated nodule. This may be followed by secondary bacterial infection causing abscessation/cellulitis. The virus multiplies in the lungs, nasal passages and lymphoid tissues fr 5 days producing a transient viraemia. Numerous skin lesions appear 10 days to several weeks later, they are oval to circular ulcerated plaques and up to 1cm in size which may occur on any part of the body. they are not pruritic.Usually resolves after 6-8 weeks.


How is diagnosis of feline cowpox made?

A positive titre is supportive of recent infection (previous 6months). Titres may be positive 7-14 days after intital exposure. crust material from skin lesions can be sent in a sterile container for analysis, pcr, viral culture or electron microscopy.


What is the cause of tuberculosis in cats?

M bovis or M microti. Most cats that are infected are keen hunters. The areas affected are the areas most likely to be bitten when playing with prey (face and front legs).


What are the clinical signs of infection with tuberculosis in cats?

Loccalised disease affecting the skin or systemic signs related to the alimentary/respiratory tracts. the most common form is the cutaneous form affecting the face, extremities, tail base or perineum. They are typically firm raised dermal nodules which may be ulcerated or form non healing wounds with draining sinus tracts. Submandibular or prescapular lymphadenopathy may be the only clinical finding. When the infection spreads to the lungs, tubercles arise in the lungs or hilar lymph nodes and affected cats present with weight loss, anorexia, dyspnoea and coughing.


How is TB diagnosed in cats?

Thorough evaluation to assess degree of systemic involvement. The IFn gamma test is good at detecting members of the tuberculosis complex. Cats do not react strongly to intra dermally administered tuberculin adn the results from intra dermal skin testing are unreliable. To confirm mycobacterial involvement, aspirates or biopsy samples hsould be stained with Zieehl Neelsen stain. While finding AFB confirms the presence of mycobacteria, it is important to culture the organism to determine the exact species involved.


You have diagnosed tuberculosis with M bovis in a cat what do you have to do?

this is notifiable to the VLA.


How should a cat with tuberculosis be managed/ treated?

Consider potential zonotic risk.
Surgical excision of small cutaneous lesions may be considered but debulking larger lesions risks wound dehiscence. Interim therapyw ith a fluoroquinolone has been recommended. This should only be considered in cases of localized cutaneous infection. initial treatment phase with rifampicin, pradofloxacin, clarithromycin, azithromycin, followed by a continuation phase of rifampicin and either pradofloxacin or clarithryomycin/azithromycin. All medications acn be given as liquids and placed in a single syringe prior to oral administration.


What is feline leprosy syndrome?

A disease caused by non tuberculosis mycobacteria, by infection form rodents (m lepraemurium) or by saprophytic usually non pathogenic organisms from the soil, water and decaying vegatation contaminating cutaneous wounds.


What are the clinical signs of feline leprosy?

Granulomatous panniculitis - multiple punctate draining tracts occur, subcutaneous nodules and coalescence produces large areas of ulcerated, non healing tissue. affected areas can be painful. the inguinal fat pads, flanks and tail base are affected most frequently.
Feline leprosy syndrome is seen as a single or multiple cutaneous or subcutaneous nodules which may be haired, alopecic or ulcerated and are typically seen on the head, limbs and occasionally trunk. they are non painful and freely mobile. regional lymphadenopathy may be present but systemic disease is rare.


How is canine distemper virus spread?

Aerosol or droplet exposure - high concentration in respiratory secretions as well as in urine and faeces.


what is the clinical outcome of CDV infection?

Depends on level of CDV antibody titres and adequacy of cell mediated immunity.
Individuals with adequate antibodies show no clinical signs although they can still shed virus. Intermediate levels results in infection of epithelial tissues and development of clinical signs, recovery is associated with long term immunity and cessation of viral shedding. Poor immune status results in severe disease and virus usually persists until death.


What are the clinical signs of CDV infection?

Bilateral discharge, coughing, dyspnoea.
Serous to mucopurulent bilateral conjunctivitis, mild anterior uveitis, degeneration/necrosis of the retina
vomiting and diarrhoea, anorexia, dehydration weight loss. Pustular dermatitis, digital hyperkeratosis
Seizures, vestibular isease, ataxia or MYOCLONUS, acute meningio encephalitis may occur in conjunction with other systemic signs. Neonatal infection prior to eruption of permanent dentition results in damage to enamel and dentine, resulting in distemper rings.


How is a diagnosis of CDV made?

Clinical signs in an unvaccinated dog especially 3-6 month old puppies. The following may be present;
Distemper inclusions on peripheral blood smears,
Non specific biochemical changes relating to dehydration, and or polyclonal gammopathy, CSF may show increased protein content and cell count, distemper inclusions on peripheral blood smears. Immunofluorescent antibody on conjunctival smears is helpful int he acute phase of the disease or on tonsilar tissue, leukocytes or respiratory epithelium. ELISA can be done on serology to detect anti CDV IgG and IgM. PCR can be performed on various tissues e.g CSF, respiratory secretions.


What is the cause of infectious canine hepatitis?

ICH is caused by canine adenovirus 1, a virus with haemagglutinating surface antigens.


How is CAV1 transmitted?

Oronasal route from infected urine, faeces and fomites. urinary excretion of virus may persist for 6-9 months after infection.


Describe the pathogenesis of canine hepatitis?

CAV1 initially localises in tonsils before progressing along the lymphatics to regional LNs and via the thoracic duct to blood. Viraemia results in dissemination to various tissues with hepatic parenchyma and vascular endothelium being the primary targets. In the liver it causes widespread centrilobular to panlobular necrosis, Dogs with high antibody titres are usually asymptomatic. A partial neutralising antibody response may develop chronic active hepatitis and subsequent hepatic fibrosis. Low level titres are associated with widespread hepatic necrosis and may be fatal. Damage to vascular endothelium results in bleeding diathesis including vasculitis and disseminated intravascular dissemination.


What are the clinical signs of infectious canine hepatitis?

Pyrexia, anorexia, vomiting, abdominal pain, diarrhoea, lymphadenopathy, hepatomegaly, jaundice, abdominal distension, petechiation, epistaxis, CNS signs depression, disorientation, seizures.


How is parvovirus transmitted?

highly contagious, infection usually results from exposure to contaminated faces. incubation is 4-14 days.


What is a common sequelae to CPV2 infection?



What are the clinical signs of Parvovirus?

Severe vomiting and diarrhoea with anorexia and rapid dehydration
Profuse foul smelling bloody diarrhoea
Pyrexia initially proceeding to hypothermia
DIC may result from gram negative septicaemia with associated haemorrhage
Neurological signs may develop as a consequence of hypoglycaemia, CNS haemorrhage, sepsis or acid base abnormalities.


How is diagnosis of pavovirus made?

Suspicion in young unvaccinated dogs with suddeon onset foul smelling foetid diarrhoea. Other organisms such as salmonella and campylobacter should be considered.
Electrolyte and acid base imbalances are common.
IDEXX cITE test - detects virus in the faeces. A negative does not eliminate possibility of parvovirus.
Serology - Rising antibody titre, haemagglutination inhibition test.
PCR detects virus antigen in faeces.
Indirect IFA on histopath samples from PM.


Which leptovirus serovar causes leptospirosis in dogs?

Leptospirosis interrogans ictohaemorrhagica
Leptospirosis interrogans canicola
Leptospirosis interrogans grippothyphosa
Leptospira interrogans pomona
Leptospira interrogans bratislava


How is leptospirosis transmitted?

Via urine, veneral and palcental transfer, bite wounds or ingestion of infected tissue.
Indirect via exposure to contaminated water sources, soil, food and bedding.


What is the pathogenesis of leptospirosis?

Leptospires penetrate mucous membranes and abraded skin and rapidly divide in the blood before spreading to other tissues including the liver and kidneys, lungs, spleen, CNS, eyes and genital tract. the extent of target organ damage depends on the dose of infection, host susceptibility and the virulence of the organism. In surviving hosts organism is shed in urine for months ot years.


What are the clinical signs of leptospirosis?

Sudden death, vomiting, rapid dehydration, cardiovascular collapse. Acute infections result in a mixture of ; pyrexia, anorexia, dehydration, polydipsia, oliguria, congested mm, jaundice, abdominal pain, paraspinal pain, anterior uveitis.


How is diagnosis of leptospirosis made?

Dark field microscopy for organism in urine, culture from urine, bloody in early acute disease. PCR in blood or urine, IFA on liver or kidney or urine, serology to demonstrate a rising antibody titre, may be negative in first 7-10 days, rising after 2-4 weeks.


What is the treatment of choice for leptospirosis?

Penicilins - immediately stop replication of the organism and reduce fatal complications. Elimination of the carrier state is achieved by administering tetracyclines, erythromycin or fluorquinolones.


What are the primary pathogens involved in canine infectious Tracheobronchitis?

Canine parainfluenza virus
Bordetella bronchiseptica
Canine influenza virus


What are the secondary pathogens involved in canine infectious tracheobronchitis?

CDV , canine herpes virus
Pasteurella, strep, pseudomonas,


What are the clinical signs of KC?

Coughing, sudden onset, retching, typically there will be a history of a visit to boarding kennels, coughing often brought on by excitement, dry or hacking cough, expectoration of mucus may occur and should be differentiated from vomiting, usually the dog is othewise healthy and active. Occasionally secondary opportunistic bacterial infection will result in the development of bronchopneumonia, mucopurulent rhinitis and conjunctivitis.


What are the requirements of the PETS travel scheme?

Pet must be microchipped.
Must be vaccinated against rabies for 21 days before travel.
Must have valid EU pet passport.
Before re entering the UK must be treated against tapeworms (between 24-120 hours before the pet is checked in with transport company). Don't need to be treated if coming from Republic of ireland, malta, finland or norway. Tapeworm treatment must contain praziquantel. (for echinococcus multilocularis)
tick treatments no longer required but strongly advised.


What is anaplasmosis transmitted by?

Anaplasma phagocytophilum are obligate intracellular bacteria transmitted by ixodes ricinus ticks. tick attachment >24hr needed for disease to occur.


What are the clinical signs of anaplasmosis in dogs?

acute onset fever, anorexia, lethargy, lameness, occasional cough, pale mucous membranes, mild to severe immune mediated thrombocytopenia. lymphopenia then lymphocytosis. can be diagnosed using Snap 4DX for A phagocytophilium, b burgdorferi, ehrlichia canis and dirofilaria. PCR on blood or synovial fluid most sensitive. tx with doxycyline.


What is lyme disease and what is it transmitted by? what are the clinical signs?

Borrelia burgdorferi, transmitted by ixodes ticks. can be transient or recurrent. clinical signs include fever, anorexia, swollen painful joints, lethargy, lymphadenopathy, immune mediated renal disease with depression, ovmiting, anorexia, PUPD. a positive PCR confirms diagnosis.tx with doxycyline.


What is ehrlichiosis and what is it transmitted by? what are the clinical signs?

Ehrlichia canis is an obligate intracellular bacteria, transmitted by ticks. E canis vector is rhipcephalus sanguineous. Acute clinical signs include pyrexia, anorexia, lymphadenopathy, bleeding diathesis, uveitis, polyarthritis. May become chronic with bone marrow infection resulting in pancytopenia. Diagnosis based on presence of intraceullar organism on blood smear, pcr, or serology. Tx with doxycyline.


What is babesia and what is it transmitted by? what are the clinical signs?

Babesia canis canis - protozoan organismm tarnsmitted by ticks, rhipcephalus sanguinous major ector. sporozoites attach to erythrocyte membrane and undergo endocytosis. haemolytic anaemia occurs due to immune mediated destruction of erythrocytes. Haemolytic anaemia associated with babesia infection has similarities with idiopathic IMHA. Autoagglutination is seen in approx 21% of cases and 85% are coombs positive. Diagnosis is by PCR on EDTA blood.


What is Leishmaniasis and how is this transmitted? what are the clinical signs/

Protozoan parasite leishmania infantum with dogs as the main resevoir, transmitted by phlebotomus sandfly and is endemic in southern europe. Clinical signs tend to arise as a result of hyperglobulinaemia and immune complex deposition and include glomerulonephritis, polyarthritis and uveitis. Infected dogs tend to become emaciated. in 90% of cases dermatological disease is present with dry desquamation and alopecia. Treatment includes allopurinol, antimonial drugs. and prevention by deltamethrin.


How does infection with dirofilariasis occur? what are the clinical signs?

Dirofilaria immitis is transmitted by mosquitos. Following infection l3 migrate to pulmonary artery where they mature to adult nematode. Clinical signs relate to presence of adult nematodes in the pulmonary arteries and range from mild exercise intolerance and coughing to dyspnoea due to allergic pneumonitis nad right sided congestive heart failure, pulmonary hypertension and syncope. Diagnosis based on detected microfilaria an antigen test which is dependent on presence of mature female nematodes, or antibody test as a screening. Treatment with melarsomine and microfilaricidal drugs such as milbemycin. Prevention with milbemycin, selamectin.


What is the pathogenesis of rabies?

following the bite, there is local viral replication in striated muscle spreading to motor nerve endings, the viral load of the bite and distance from the brain will affect how long it takes for clinical signs to appear. virus spreads inspinal cord neurons, rapid spread to CNS causing progressive paralysis of lower motor neurons, viral spread through peripheral and cranial nerves into other tisues including salivary glands but also kidneys, eyes, skin, adrenal glands.


What are the clinical signs of rabies?

Prodromal phase - lasts for around three days, subtle behavioural changes, sensitivity to noise/light, biting/licking of wound, anorexia.
Dromal phase - in furious form there is aggressive ,attacking animals, agitation, convulsions, vocalisation, drooling.
In the dumb form; dullness, dyspnagia, profuse salivation, dropped jaw, prolapsed third eyelid, beginning of paralysis.

Paralytic phase - progressive paralysis of hind limbs, staggering gait, paralysis of swallowing muscles, foaming at the mouth, severe respiratory difficulties, lapsing into a coma and death.


What is the gold standard test for rabies?

Fluorescent antibody test on brain tissue
Also rabies tissue culture inoculation test for confirmation, examine inoculated tissue after 3-4 days using FAT.


What is the cause of bat rabies?

European bat lyssavirus 2. evidence suggests that bats can recover form EBLV or assume silent carrier status. method of transmission is similar to terrestrial rabies. clinical signs include incoordination and abnormal behaviour e.g active during daylight hours.


If you have a dog with a lesion in the left vestibular system, which way will it circle?

Inhibit contralateral antigravity muscles so head body eye tilt circling TOWARDS lesion - will circle towards left.


What are the clinical signs of a brainstem lesion?

Dropped jaw
Changed facial sensation
Paralysis of eyelid, lip or ear
Laryngeal paralysis
Head tilt, circling, nsytagmus


What signs would you expect to see with a cervical lesion?

Ataxia in all limbs with good reflexes


What would you expect to see with a lesion from c6-t2?

Poor reflexes in thoracic limbs, ataxia in pelvic limbs


What would you expect to see with a lesion from t3-t12?

ataxia with good reflexes in the pelvic limbs


What would you expect to see with a lesion from t13-L2?

good reflexes in thoracic limbs, poor reflexes in pelvic limbs


What are the clinical signs of forebrain disease?

abnormal behaviour - apathy, aggresion, failure to recognise the owners, loss of trained habits, staring at walls, getting stuck in corners, abnormal mental status, disorientation, stupor, coma, circling in wide circles toward the side of the lesion, continuous pacing, normal gait with delayed postural reactions in contralateral limbs. impaired vision in the eye contralateral to lesion and normal PLR, facial sensory deficits, head turn towards side of lesion, generalised seizures, partial seizures,


What are the clinical signs of lysosomal storage disease? what breeds are these common in?

Most inherited as autosomal recessive, clinical signs of diffuse neurological dysfunction evident before 1 year of age, progressive leading ot premature death.
Laforas disease in beagle, basset hound or other breedsm Fucosidosis - springer spaniels
Ceroid lipofuscinosis - english setter, cocker spaniel, dalmation, dachshund.


What can be used as a treatment for hydrocephalus?

Diuretics such as furosemide, corticosteroids, and other carbonic anhydrase inhibitors such as acetozalamide to decrease CSF production.


When should a brain tumour be suspected?

In an older animal with progressive neurological signs or pets > yo with sudden onset of seizures. some breeds such as boxer have higher incidence.
Gliomas most common in brachycephalic dogs and meningiomas in doliocephalic dogs.


What is granulomatous meningoencephalitis and what are the clinical sgns?

subacute, chronic non suppurative inflammation of the CNs, commonly affecting female middle age small breed dogs. unknown aetiology, suspected immune disorder. Three clinical forms: disseminated, focal and ocular.


What is necrotizing meningoencephalitis?

Described mainly in pug dogs, amltese dogs and yorkshire terriers but also in other small breeds such as chihuahuas. The necrotizing meningoencephalitis in pug and maltese dogs affects young dogs with a chronic and progressive course characterized by seizures poorly responsive to anticonvulsant drugs. Yorkshire terriers are affected between 1 and 10 yo and the clinical signs are associated with a brainstem lesion usually. prognosis is poor, corticosteroid and anticonvulsant therapy provides only a temporary improvement.


What is the treatment for ethylyene glycol toxicity?

4MP for dogs, ethanol for cats.


What are the goals of head trauma management?

Maintain ventilation, avoid hypotension, prevent/treat cerebral edema, treat increased intracranial pressure


What is cheyne stokes respiration?

periods of hyperventilation which taper off gradually to periods of apnea of variable duration. when respiration resumes gradually accelerates to the point of hyperventilation. lesion in deep cerebral hemispheric structures, basal ganglia and diencephalon.


What is decerebrate rigidity?

Unconscioussness> abnrormal PLR > opisthotonus > extension of thoracic and pelvic limbs


What is decerebellate rigidity?

Alert, normal PLR, opisthotonus, extension of thoracic limbs, extension or active flexion of pelvic limbs.


What are the clinical signs of increased ICP?

Nausea/vomiting, decreased PLR, decreased level of conscioussness, cushings reflex - hypertension and bradycardia, abnormal respiratory pattern, increased limbs extensor tone


What is cushings reflex?

Increased ICP decreases cerebral perfusion pressure and cerebral blood flow, inducing cerebral ischaemia, ischaemi triggers a sympathetic response causing elevated heart rate and systemic extracranial vasoconstriction to push more blood to the brain and improve its perfusion > reflex systemic hypertension > severely elevated systemic arterial blood pressure will stimulate the carotid baroreceptors which in turn slow down the heart rate > reflex bradycardia.


What are the typical signs of a tonic clonic seizure?

Animal suddenly gets stiff and unresponsive, then falls in lateral recumbency with rigid extension of the front limbs, and the head and neck become rigidly extended backward, symmetrical orofacial movements may precede the tonic phase. the patient can be apneic for a while, the eyes are usually open and the pupils are mydriatic, jaw could be wide open or clenched, paddling movement when clonic phase starts, drooling, urination/defecation, then relaxes.


What are cluster seizures?

More than two seizures in a 24 hour period or over 2-3 consecutive days.


what is status epilepticus

A seizure that shows no clinical signs of arresting after 5-10 minutes ofa ctivity or recurrent seizures with no recovery of normal/baseline neurological functions between them.


Which drugs should be avoided in epileptic animals?

Phenothiazines such as acepromazine, metoclopramide, penicilin, chloramphenicol, enrofloxacin and estrogens or testosterone, may lower seizure threshold.


Which direction does a pathologic nystagmus go to?

The pathologic nystagmus has the fast phase directed AWAY from the lesion. (the exception is the paradoxical vesticular disease in which a central vestibular lesion could induce nystagmus with fast phase toward the side of the lesion')


What are the symptoms of horners syndrome?

Enopthalmos, protruding third eyelid, ptosis, miosis and sweating of the ipsilateral face in horses. it is caused by a lesion in the sympathetic innervation of the eye. the sympathetic nerve courses through the middle ear in dos and cats and is often affected in otitis media.


What is old dog vestibular syndrome?

Acute, idiopathic, peripheral vestibular disease associated with vomiting, nausea, severe vestibular deficits. in 3-2 days there is spontaneous improvement and usually back to normal in 7-10 days. in some cases it takes up to 2-3 weeks. residual head tilt possible, recurrence possible.


What are the possible side effects of metronidazole toxicity?

Vestibular ataxia, vertical nystagmus, anorexia


What are the cranial nerves?

I - olfactory - smell
II - optic- vision and PLR
III - oculomotor - innervates parasympathetic fibers for constriction of pupil, dorsal medial and ventral recti m.
IV - trochlear - medio ventral rotation of eye (dorsal oblique extraocular m)
V - trigeminal N - sensation to eye and cornea, sensation to maxillary and mandibular, motor inervation to muscles of mastication.
VI - abducens - lateral movement of eye through innervation of lateral rectus m. rectraction of eye bulb.
VII - facial- motor to muscles of facial expression, taste, salivation, skin sensation of ear
VIII - vestibulocochlear - balance and posture, eheairng
CN IX - glossopharyngeal - motor and sensation to pharynx, taste, salivation
CN X - vagus n. motor and sensation to larynx, taste ,salivation, parasympathetic innervation to viscera.
CN XI - accessory n.motor to trapezius m.
CN XII - hypoglossal n. motor to the tongue.


How can you locate a lesion with a blind animal?

If the animal is blind but the PLRs are intact the lesion is after the optic tracts, in the contralateral cerebral hemisphere.
If the animals i blind and PLR is absent the lesion is in the eye itself, optic nerve, optic chiasm or optic tract.


How is potassium bromide excreted?

Via kidneys


How do barbiturates and benzodiazepenes work against seizures?

They have enhanced GABA synpatic transmission (gaba agonists)


How does potassium bromide work against seizures?

Crosses neuronal Cl- channels more readily than Cl-. Gaba enhances this influx of bromide leading to neuronal hyperpolarization thus bromide stabilizes neurones against excitatory input from epileptic foci. Halide element and causes neuronal hyperpolarization by entering neurons via chloride channels. it is synergistic with phenobarbital.


Does epilepsy occur in cats?

Much less common than in the dog, more often reflects structural disease, metabolic tolerance to phenobarbital does not occur. Diazepam has been used for maintenance therapy in the cat.


What are the clinical signs of cerebellar disease?

Cerebellar ataxia - failure of motor coordination, broad base stance hypermetria and titubation
titubation - swaying of body
dysmetria - high stepping gait
intention tremors
vestibular signs
decreased or absent menace
increased muscle tone and normal to exaggerated spinal reflexes
delayed postural reactions


What is cerebellar abiotrophy?

Neurons in the cerebellum develop and differentiate normally but then start to degenerate and die prematurely. seen in kerry blue, gordon setter, rough coated collie, brittany spaniel. Normal gait at the time they begin to walk. clinical signs are insidious onset, progressive and symmetrical.


What is cerebellar hypoplasia?

Cerebellar malformation, associated with genetic disorders, in utero viral infections or toxins. Neurological deficits are apparent in the animal at first attempt to ambulate. not progressive and some animals may learn to compensate. Commonly associated with feline panleukopenia virus, canine herpes virus and bovine viral diarrhoea.


How can you localise the lesion in a the spinal cord of an ataxic dog?

Ataxia with intact reflexes present in all 4 limbs : c1-c5

ataxia in all limbs, Decreased reflexes in thoracic limbs, present in pelvic limbs c6-t2

Thoracic limbs normal, pelvic limb ataxia with intact reflexes t3-l3

Thoracic limbs normal, reflexes decreased decreased in pelvic limbs - LS intumescence

Reflexes absent in all four limbs - Diffuse LMN


What is the difference between type I and II hansen disc disease?

I - extrusion only, chondrodystrophic breeds, young (3-6yo), risk of rupture of annulus & herniation of nucleus pulposus into vertebral canal.

II - protrusion only, non chondrodystrophic breeds, older dogs, fibrous degeneration.


What is fibrocartilagenous embolism?

Sudden onset disease in mostly non chondrodysplastic dogs, non painful, non progressive. source of cartilage is unknown, treatment is conservative.


What is meningitis arteritis?

More common in young, large breed dogs and colony beagles. causes sudden onset extreme pain, commonly obtunded, pyrexic, suppurative leptominngitis/arteritis. most dogs respond well to high dose steroids. Bacterial meningitis v uncommon in small animals.


What is discospondylitis?

Pyogenic vertebral osteomyelitis. Common in young to middle aged dogs. Present with pain and plegia. The resulting erosive lesions of the intervertebral disc and the vertebral body endplates may result in instability, extradural spinal cord or cauda equina compression due to granulation tissue, collapse of the intervertebral space and/or pathological vertebral fractures or luxation.


What is degenerative myelopathy?

seen in GSD >5yo, causing progressive paraparesis and tetraplegia, widespread demyelination of the spinal cord, most severe in T-L region, no treatment and prognosis is poor.


What condition are king charles cavalier spaniels prone to?

Caudal occipital malformation syndrome and subsequent syringomyelia has been commonly reported in Cavalier King Charles Spaniels and less commonly in other small breed dogs. The malformation is comparable to the Chiari type-I malformation described in people and includes a congenital malformation of the occipital bone, resulting in a crowded caudal fossa and cerebellar herniation at the foramen magnum. The subsequent disruption of CSF flow results in formation of syringomyelia. A large proportion of asymptomatic Cavalier King Charles Spaniels have the caudal fossa malformation. Although the malformation is present at birth, clinical signs often do not appear until later in life. Clinical signs vary but commonly include paresthesias (eg, face rubbing, phantom scratching of the back of the head), ataxia, and weakness from syringomyelia. Medical management is often not curative but can be attempted with gabapentin (10 mg/kg, PO, tid) for paresthesias, omeprazole (0.7 mg/kg/day, PO) for reduction of CSF production, and analgesics for pain management. Surgical decompression via caudal occipital craniectomy is preferred as definitive treatment; however, recurrence rates of 25%–47% have been reported.


What is polyradiculoneuritis?

An inflammatory condition primarily involving multiple nerve roots, with sudden onset of paresis, paralysis or tetraplegia, some appear to be hyperaesthetic, cranial nerve involvement ay be prominent. associated with a racoon bite. ''coonhound paralysis''


How does botulism toxin work?

Toxin binds on nerve terminal and is internalised into the vesicle. botulinum toxin remains at neuromuscular junction and prevents acetylcholine exocytosis.


How does tetanus toxin work?

Internalised by inhibitory interneuron > inhibits release of glycine and gaba.


What is myasthenia gravis?

Presynaptic, synaptic or post synaptic defects in neuromuscular transmission. Congenital and acquired forms present. Acquired form usually associated with serum antibodies to nicotinic acetylcholine receptors. sometimes associated with thymoma. many go into spontaneous remission. Csx - exercise related appendicular muscle weakness, megaoesophagus, laryngeal/pharyngeal muscle weakness.


How is myaesthenia gravis diagnosed?

Anticholinesterase challenge test - tensilon
anti achr antibody serology


what is the treatment for acquired myaesthenia gravis?

Anticholinesterase - pyridostigmine bromide, immunosuppressants


What is dermatomyositis?

Causes facial dermatitis and mild generalised myositis in collie dogs, poor response to treatment.


What are the common presenting signs with heart disease in dogs?

Coughing caused by left atrial enlargement. May be one of the first signs noted in chronic mitral insufficiency or DCM.
Dyspnoea is generally associated with congestive heart failure. it may be caused by pulmonary oedema (left sided heart failure) or pleural effusion (right sided heart failure). It may also be present with right to left shunts, and with pericardial effusions.
Exercise intolerance
Syncope - occurs on exertion or excitement, no warning signs, short duration, lack of salivation, vocalisation, urination, defecation, tonic clonic spasms, rapid recovery.
Abdominal enlargement - right heart failure may result in hepatic congestion and secondary ascites, in some animals this may be the first sign noticed by the owner.
Weight loss common with biventricular failure.


What are the common presenting signs with heart disease in cats?

Cats with left atrial enlargement rarely present coughing, they usually present with dyspnoea as pulmonary oedema develops.
Exertional dyspnoea may be present in cats but not observed by the owner because of the cats reluctance to move.
Weight loss common with biventricular failure.


What is vertebral heart scoring? what should be the size of the dog and cat heart?

The width and length of heart is measured on the lateral view against the number of vertebral bodies starting at t4. then added together. average in dogs is 9.7 (8.5-10.5 normal) and cats should not exceed 8.


What conditions may commonly cause left atrial enlargement?

Mitral insufficiency, dilated cardiomyopathy, hypertrophic cardiomyopathy, PDA.


What conditions commonly cause left ventricular enlargement?

Mitral insufficiency, endocardiosis, mitral dysplasia, dilated cardiomyopathy, hypertrophic cardiomyopathy, patent ductus arteriosus, ventricular septal defect.


What conditions cause right atrial enlargement?

endocardiosis, pulmonic stenosis, dilated cardiomyopathy, restrictive cardiomyopathy.


How does the pulmonary parenchyma appear on radiographs in dogs with heart failure?

The interstitial tissue of the lungs becomes more prominent in interstitial pulmonary oedema. this appears as an ill defined increase in density starting in the hilar area in dogs, which may blur underlying markings. Cats tend to have a more generalised or patchy appearance. alveolar markings may develop in severe pulmonary oedema, once alveolar flooding has occurred. In severe cases the only lucent areas will be in the bronchi which will be black and surrounded by soft tissue density 'air bronchograms'


What is the P wave?

Depolarization of atria in response to SA node triggering.


What is the QRS complex?

Depolarization of the ventricles, triggers main pumping contractions


What is the T wave?

Ventricular repolarization.


Which leads are placed on which limbs for ECG?

Red - right forelimb
Yellow - left forelimb
Green - left hindlimb
Black - right hindlimb


What does a P wave without a QRS complex signify?

Indicates atrial depolarization, which has not been conducted through the atriventricular node to the ventricles. i.e AV BLOCK.
Long PQ interval - First degree AV block.
No consistent relationship - third degree av block


What does a QRS complex without a p wave signify?

There are either ectopic complexes, atrial fibrillation or sinoventricular complexes.


What does a Wide P wave signify?

Left atrial enlargement


what does a tall P wave signify?

right atrial enlargement


What does a wide QRS Complex signify?

Left ventricular enlargement or left bundle branch block


What does a Tall R signify?

Left ventricular enlargment


What does a small R signify?

Pericardial/pleural effusion


What do alternate R waves of different heights signify?

Pericardial effusion


What does a deep S wave signify?

Right ventricular enlargement


When is a long Q-t seen?

In hypocalcaemia, hypokalaemia, hypthermia.


what is sinus arrhythmia?

Heart rate varies with respiration, normal P waves and normal QRS complexes. not a normal rhythm in cats.


What is sinus arrest?

No evidence of atrial activity for a period in excess of the two proceeding r-r intervals. If the period of block is an exact multiple of the proceeding R-r intervals then sinus block is more likely. Recognised in dogs with high vagal tone e.g brachycephalics with underlying respiratory disease. Ventricular escape beats may be recognised. If related to high vagal tone - should be easily abolished with atropine.


What is sick sinus syndrome?

Common in min schnauzers. Periods of sinus arrest without appropriate escape beats. no response to atropine. Spuraventricular tachycardia may occur. Most cases present because of syncope.


What is sinus bradycardia?

May be a normal rhthmn, may also be recognised in patients with hypothermia, hyperkalaemia, cns lesion, digoxin toxicity or high doses of calcium channel antagonists.


What is atrial standstill?

No atrial activity and no p waves. heart rate is slow. QRS complexes may be wide and bizarre. this is associated with hyperkalaemia,


What is the difference between 1st degree AV block, 2nd degree AV block and 3rd degree AV block?

1st - conduction across AV node is slowed. Pq interval is long.
2nd - Some of P waves are not conducted across the AV node and do not result in QRS complex. In mobitz Type I, the P-r interval may be variable, increasing prior to a block. in Mobitz type II the P-R interval is constant. this is generally more serious.
3rd - no conduction across the AV node. the p waves are not associated with the QRS complexes. There tends to be a constant and regular P wave rate. The ventricles beat at a regular escape rate, which is much lower than the P wave rate. These cases usually tend to present with syncope due to slow heart rate. This may be idiopathic or due to fibrosis occuring in the AV node. tx of choice is pacemaker implantation.


What is supraventricular tachycardia?

If more than 4 premature supraventricular beats occur together this is called a run of supraventricular tachycardia. It is caused by atrial stretch or infiltration.


What is atrial fibrillation

A chaotic rhythm where several foci are discharging at the same time in the atria. there are no recognisable P waves. the QRS complexes are of normal morphology as conduction is through the Av node. the rate is frequently rapid and irregular. This is caused by atrial stretch in small animals and is commonly seen with DCM. On clinical exam there is a marked pulse deficit.


What is a ventricular premature complex?

Complexes occur early and are wide and bizarre in appearance as they are ventricular in origin, no associated P wave, may occur with primary cardiac disease or due to stretch, hypoxia or infiltration of the ventricular wall. Frequently associated with systemic disease e.g GDV, splenic mass, CNS disease.


What is ventricular tachycardia?

More than 4 premature ventricular complexes occuring together Aetiology is the same as for ventricular premature complexes. Treat with iv lignocaine, then oral procainamide, mexiletine .


What are ventricular escape beats?

These occur late. they are wide and bizarre in appearance. there is no associated P Wave. they are rescue beats and should not be suppressed.


What is the treatment for atrial fibrillation in dogs?

Beta blockers
Calcium cahnnel blockers.


Which breeds is idiopathic pericardial effusion common in?



What are the clinical signs of a pericardial effusion? and on ECG?

Heart sounds are muffled, jugular veins distended, pulse frequently weak and pulsus paradoxus may be present. The R waves may vary in height (electrical alternans), this reflects the swinging of the heart in the pericardial fluid.


What is the treatment for pericardial effusion?

Periocardiocentesis on first presentation but recurrence is common and is best treated by sub total pericardectomy. Diuretics should be avoided as may lead to severe hypotension. Periocardiocentesis best through 5-6th intercostal space. The effusion is typically haemorrhagic however it does not clot and thus can be differentiated from ventricular blood.


What is the pathophysiology of infection with angiostrongylosis?

The adult worm - angiostrongylus vasorum, parasitise the pulmonary artery and right ventricle. Eggs are laid in the pulmonary parencyma and hatch to first stage larvae and enter the airways, and are coughed up swallowed and passed in the faeces. Snails or slugs act as intermediate hosts as they ingest alrvae from dog faeces. a dog becomes infected by eating infected snails or slugs. From the intestine the larvae migrate through the lymphatic system or hepatic portal vessels to the right heart. Rare in scotland. Crenosoma more widespread.


What are the clinical signs of lungworm infection?

Many are subclinica. coughing may be the most common clinical presentation with a duration of a few to several months. additional clinical signs include weakness, subcutaneou swelling, lameness, anaemia, pulmonary crepitation, right sided heart failure, collapse, dspnoea, respiratory distress. Stage 1 larvae can usually be found in the faeces.


What is the treatment for lungworm?

fenbendazole and moxidectin


What is the pathophysiology of dirofilariasis infection? (heartworm)

Infection of the pulmonary arteries and occasionally right heart by the nematode dirofilaria immitis. Life cycle of D immitus must pass through a female mosquito. Maturation time in the mosquito is 10-14 days in optimal conditions. Once injected into the host the larvae migrate in tissues and moult, the final maturation phase int he pulmonary arteries takes a further 3-4 months. Female worms produce microfilaria that pass into the circulation. the presence of parasites in the pulmonary arteries leads to local changes in blod vessels and can lead to pulmonary hypertension. pulmonary hypertension may result in right sided congestive heart failure.


What are the clinical signs of heartworm infestation?

Coughing, dyspnoea, tachypnoea. Exercise intolerance, syncope, haemoptysis, ascites and hepatomegaly also reported. Rarely dogs may present with caval syndrome, large number of worms in right ventricle causing poor cardiac output and intravascular cell lysis.


which dogs are predisposed to aortic stenosis?

Boxers, German shepherd dogs, newfoundland, rottweiler and golden retrievers.


What wil be heard on auscultation with aortic stenosis?

Systolic ejection type murmur loudest over the left heart base, radiates up the carotid arteries. murmur intensity correlates with severity of the stenosis.


What effect does aortic stenosis have on the heart? How is this seen on ECG?

Left ventricular wall thickening, abnormal valvular or subvalvular anatomy, increased outflow velocities on doppler echocardiography. Velocities are used to grade the stenosis into mild, moderate and severe. On electrocardiography - left ventricular enlargement, increased R wave amplitude and QRS duration, myocardial hypoxia, ventricular arrhythmias.


What is the treatment for aortic stenosis?

Prophylaxis for bacterial endocarditis, exercise restriction, adrenergic blocking drugs indicated in moderate to severe cases.


What does the ductus arteriosus do in the foetus?

Connects the main pulmonary artery to the aorta in the foetus.


How does polycythaemia occur in PDA?

Blood from systemic circulation flows into the pulmonary vasculature. There is pulmonary enlargement and decreased pulmonary compliance. Large defects may develop severe pulmonary hypertension, which causes shunting of unoxygenated blood from the pulmonary artery into the systemic circulation which causes chronic hypoxia resulting in increased erythropoietin release by the kidneys, increased RBC production by the bone marrow and the development of polycythaemia.


Which breeds are predisposed to developing PDA?

King charles cavaliar spaniels, poodles, german shepherd dogs, springer spaniels, collies, shetland sheepdogs, pomeranians.


what is heard on auscultation of a PDA?

A high grade, continuous machinery heart murmur audible over the left heart pase. steep water hammer pulse, right to left shunting defects may have no audible murmur.


What effect does PDA have on the heart and how does this show on ecg?

Lef atrial enlargement, wide P waves, left ventricular enlargement, tall wide R aves, arrhthmias including atrial and ventricular premature complexes and atrial fibrillation.


what is the treatment of PDA?

Occlusion of the ductus by surgical ligation or transvenously using a variety of occluding devices. left sided congestive heart failure may require management with diuretics and ACE inhibitor therapy.


What breeds are predisposed to pulmonic stenosis? What does this murmur sound like?

Miniature schauzers, boxers, beagles, bull mastiffs, bull dogs, cocker spaniels, chihuahuas. Harsh, left base systolic murmur, often radiates across to the right heart base.


What does mitral valve dysplasia sound like?

Harsh pansystolic murmur audible loudest over the left apex.


What does tricupspid valve dysplasia sound like?

Harsh systolic murmur audible loudest over the right apex, jugular venous distension and pulsations may also be noted on clinical examination. right atrium markedly enlarged.


What is the most common congenital cardiac abnormality of cats?

Ventricular septal defect.


what is the sequelae to ventricular septal defect?

Left ventricle to right or less commonly from right to the left.


What does tetralogy of fallot consist of?

Four different abnormalities, ventricular septal defect, pulmonic stenosis, right ventricular hypertrophy and an overriding aorta. results in right to left shunting of blood and resultant chronic hypoxia.


What breeds are prone to DCM?

Great Dane, wolfhound, Newfoundland, Irish setter, Doberman, cocker spaniel


What chemotherapeutic agent may cause DCM?



What is heard on auscultation with DCM?

Low grade apical murmur, diastolic gallop, sinus tachycardia arrhythmias common, atrial fibrillation in Irish wolfhound and Great Danes


What is present on ecg with DCM?

Left atrial enlargement - wide P waves and left ventricular enlargement - tall r waves, wide QRS, st coving


What treatments are used for DCM?

Pimobendan- an inodilator (positive INotrope and vasodilator.


Why is feline dilated cardiomyopathy rare now?

As taurine is added in commercial cat foods


What breeds are prone to DCM?

Great Dane, wolfhound, Newfoundland, Irish setter, Doberman, cocker spaniel


What chemotherapeutic agent may cause DCM?



What is heard on auscultation with DCM?

Low grade apical murmur, diastolic gallop, sinus tachycardia arrhythmias common, atrial fibrillation in Irish wolfhound and Great Danes


What is present on ecg with DCM?

Left atrial enlargement - wide P waves and left ventricular enlargement - tall r waves, wide QRS, st coving


What treatments are used for DCM?

Pimobendan- an inodilator (positive INotrope and vasodilator.


Why is feline dilated cardiomyopathy rare now?

As taurine is added in commercial cat foods


What two common conditions may result in secondary hypetrophy of the heart in the cat?

Hypertension - check renal function and systemic BP
And hyperthyroidism


What is the treatment for hypertrophic cardiomyopathy?

Beta blockers or calcium channel antagonists act as negative chronic ropes and negative inotropes resulting in improved diastolic filling diuretics and ace inhibitors indicated in congestive heart failure and aspirin every 3rd day or daily clopidogrel.


Why does thromboembolism commonly occur in cats?

They have a high platelet mass/kg body weight and platelet aggregation occurs readily. Blood stasis occurs in left atrium in myocardial disease leading to thrombus formation. Emboli zeroing commonly occurs to external iliacs and renal arteries


What are the clinical signs of thromboembolism in the cat? How can it be treated?

Hindlimb paresis, severe pain, spasm of muscles, cyanotic nail beds, absence of femoral pulse.

Analgesia, sedation, possible ACP, heparin to prevent further embolism, aspirin or clopridogrel, circulatory support but be v careful if congestive heart failure is present. Treat underlying disease. Physiotherapy. Prognosis guarded. Limb fiction returns after 14 days but many have recurrences.


What is boxer dog cardiomyopathy?

Arrythmogenic right ventricular cardiomyopathy in boxers. Causes sudden death. Genetic component . RIGHT Ventricle is replaced by fibrous tissue.


Which valve is most commonly affected in bacterial endocarditis in small animals?

Left side of the heart - septic emboli are seeded to the joints and kidneys. In dogs periodontal disease may be a major primary source of infection.


What is glyceryl trinitrate?

Useful in cardiogenic pulmonary oedema. It is a venodilator, absorbed through the skin. Short term therapy only


How does pimobendan work?

It is a phosphide stress inhibitor and calcium sensitiser. Calcium sensitisation without increased myocardial oxygen consumption probably most important for myocardial effect. It is orally bio available but is reduced in the presence of food, administered BID one hour prior to feeding.


What is dobutamine?

A synthetic b1 adrenergic agonist, minimal b2 or a2 adrenergic effects. B1 adrenergic stimulation - increase in adenylyl cyclase - increase in camp- protein kinase A - increase in intracellular calcium. The main indication is in severe acute heart failure with poor left ventricular function. Also used in horses during anaesthesia to maintain MAP.


What is the purpose of vasodilators? (E.g pimobendan, ace inhibitors, calcium channel blockers)

Aim to decrease the preload and after load, results in reduced cardiac workload and congestion.


How do ACE inhibitors work?

Block effects of angiotensin II. Eg enalapril, Benazapril. Several months before benefits of ACE seen.


What is amlodipine?

A calcium channel antagonist


How does quinidine work?

It is a Class 1a anti arrythmogenic. It increases SA node discharge and conduction. It is used in atrial fibrillation in the heart, ventricular tachycardia in the horse.


How does Lidocaine work?

It is a class 1B anti arrythmogenic. It increases the ratio of ERP to AP duration, accelerates repolarisation and decreases automaticity and conduction velocity primarily in diseased tissue. It is the treat of choice for emergency treatment of life threatening ventricular arrhthmias.


What is mexiletine?

a class 1b anti arrythmogenic. it has similar properties and effects to lidocaine.


What is atenolol and what is it used to treat?

B1 selective antagonist - B blocker. It is selective for b1 adrenergic receptors in the heart so minimal vasodilatory or bronchoconstrictive effects. Can all cause hypotension and bradycardia. the transient hypertension may be reported at the start of treatment.


What is sotalol?

Has beta blocker and K+ channel blocker effects, prolongs action potential duration and decreases automaticity, slows AV conduction and refractorinessm eliminated via the kidney unchanged.


How do calcium channel blockers work?

Block the slow calcium channels, and have a profound effect on nodal tissue, slows sinus rate, speed of conduction and induces vasodilation. e.g Diltiazam, verapamil and amlodipine.


What is digoxin?

A cardiac glycoside - causes positive inotorpy and negative chronotrophy.


what is the treatment for bradydysrythmias?

Usually more long term abnormalities due to disease within the heart and tend to respond poorly to medical management but pacemaker is the treatment of choice. Condition may be due to something else e.g hyperkalaemia. Drugs that can be used include muscarinic antagonists e.g atropine and glycopyrronium.


How do thiazide diuretics work? what are the side effects?

the main site of action is the Distal convoluted tubule, they are excreted in to the PCT and need to be in the tubule to exert an effect. moderate diuretics due to site of action. inhibit the Na/cl co transport system by binding to it. They prevent sodium and chloride ion reabsorption but much sodium has already been reabsorbed by this time. They increase the loss of K+ since more sodium is presented in the collecting tubule and more urine flow due to increased volume. They are used for mild cardiac failure to manage oedema, and can be combined with other diuretics e.g furosemide. Generally quite safe, main side effect is hypokalaemia. Decrease effect of insulin.


What diuretics are sometimes used to treat diabetes insipidus? How does this work?

thiazide diuretics - mechanism of thiazides unclear. D insipidus can be central or nephrogenic. central form vasopressin treatment of choice. Thiazides - loss of sodium and water in the DCT leads to hypovolaemia. More sodium and water reabsorbed in the PCT. Less urine in the loop of helne > less urine presented to the collecting tubule.


How do loop diuretics work?

Site of action is the thick ascending loop of henle > inhibit the cotransport of Na+K+/2cl from the lumen into the tubule cell. This reduces the hypertonicity of the medulla responsible for the reabsorption of water from the collecting tubule and the descending loop of henle, which results in a dramatic increase in water loss by the kidney. potassium also lost due to decreased reabsorption in the ascending loop and also increased sodium presentation in the collecting tubule. Ca2+ loss is increased also.


What are the uses of loop diuretics e.g furosemide?

Heart failure for the management of oedema, given i/v vasodilationc an help to reduce preload and increase renal perfusion. treatment of hypercalcaemia since promotes calcium loss.


How does spironolactone work?

It is an aldosterone antagonist. since it inhibits the effects of aldosterone the effect is a loss of sodium and water and the retention of potassium.


What is amiloride?

A potassium sparing diuretics. prevents the reabsorption of sodium through the luminal sodium channels. Reduces the loss of potassium and increases the loss of sodium. Potassium sparing effect is greater where potassium loss is elevated. There main use is in conjunction with other diuretic agents in the management of severe cardiac failure. used with furosemide since it complements the potassium loosing effect of this diuretic.


What type of diuretic is mannitol?

an osmotic diuretics. it is freely filtered by the glomerulus. As Na and water are removed in the PCT the mannitol becomes progressively concentrated. It reduces the rebabsorption of water int he PCT. Na + remoal then declines. Prostaglandin release enhances the renal medullary blood flow reducing the hypertonicity of the medulla. It is used in the management of acute renal failure to restore urine production, used to reduce CSF pressure, used to reduce intraocular pressure in glaucoma.


What are carbonic anhydrase inhibitors and what are they used for?

Carbonic anhydrase allows the reformation of Hco3- and H+ > H2o and Co2. The net effect is the reabsorption of HCO3- from the PCT. when carbonic anhydrase is inhibited, bicarbonate stays in the lumen together with NA+ and K+. This causes a rise in urine volume and an increase in the urinary pH. Metabolic acidosis ensues due to the reduced HCO3 which in turn reduces the actions of the diuretics.


What is acetazolamide used for?

It is a carbonic anhydrase inhibitor, used to treat glaucoma since carbonic anhydrase on the ciliary epithelia is involved in the formation of aqueous humour.


What signs may eyelid abnormalities show in dogs?

Corneal ulcers, neovascularisation and pigmentary keratitis.


Waht is the most common site of entropion?

Lateral lower lid


What is the treatment for entropion??

Excisional correction not always required in younger patients where there is still considerable anticipated growth but a temporary procedure is necessary to relieve discomfort and prevent damage to the cornea. Vertical mattress sutures or vertically orientated surgical staples are left in place for a few weeks but may be all that is required in a younger patient, particularly the sharpei. For simple anatomical entropion the Hotz celsus technique is straight forward and effective.


What is atonic entropion/trichiasis?

loss of tone in the skin of the upper eyelid, combined with an excessive amount of head skin, can result in the lateral upper lid drooping to the extent that hairs and cilia impinge on the cornea causing discomfort and corneal damage. This is common in cocker spaniels. best treated with the stades procedure.


What is distichiasis?

A very common condition where abnormally positioned cilia emerge form the lid margin, usually at or close to the tarsal gland openings. Most show no clinical signs. Corneal ulceration has been reported but v rare. electrolysis or cryosurgery can be performed. The hairs will regrow if plucked but this will allow the significance of the distichiasis hairs as a source of irritation to be determined.


What are conjunctival cilia?

Much less common than distichiasis - usually a single hair emerging through the palpebral conjunctiva a few millimetres from the lid margin at right angles to the cornea. very painful. Frequently there is a shallow, vertically orientated ulcer opposite the emerging cilia. Treatment is by excision of a wedge of tissue containing the cilium from the conjunctival surface.


What is trichiasis?

Periocular hairs growing in a normal location which may be directed abnormally towards the ocular surface, which may cause conjunctivitis and keratitis. trichiasis results form entropion and can be associated with nasal folds, medial canthus and caruncle.


What is the most common eyelid tumour in dogs?

Tarsal adenomas, followed by melanomas. most are benign but may abrade the cornea or bleed and should be removed if causing problems.


What is cherry eye?

Dorsal prolapse of the nictitans gland - smooth pink swleling at the medial canthus. The mass is seen to protrude from behind the leading edge of the membrane. this is seen in young dogs, especially cocker spaniels, beagles and bracycephalic breeds as well as mastiffs and great danes.


what is the treatment for prolapse of the nictitans gland?

Although the gland can be excised, there is an unacceptably high post operative risk of ry eye. surgical replacement should therefore be attempted. two techniques include the pocket technique and the anterior anchoring technique. care should be taken with suture placement in the pocket technique to avoid corneal damage.


What is plasma cell infiltration of the third eyelid?

A condition affecting the GSD and collie types, with bilateral depigmentation of the membranem a pink/red fleshy infiltrate and a rough irregular surface. the infiltrate consists of plasma cells and lymphocytes and is often concurrent with chornic superficial keratitis. there is usually minimal discomfort. tx is ith topical corticosteroids and cyclosporine may also be used.


What is opthalmia neonatorum?

Infection within the ocnjunctival sac before the eyelids are opened - usually at 10-15 days


What is the cause of keratoconjunctivitis sicca?

Resulting from a deficiency in the aqueous portion of the tear film produced by the lacrimal and nictitans glands. caused by immune mediated destruction of the lacrimal tissue with progressive loss. the great majority of cases are immune mediated. most commonly seen in westies, cocker and CKCS, shi tzu, lhaso apso. It can be drug induced due to Sulphonamide antibiotic (sulphadiazine and sulphasalazine)


What is the normal schiermer tear test value?

>15mm is normal. Mean normal is around 21mm in the dog. values of 12-15 should be interpreted on the basis of ocular surface appearance and level of discomfort.


What are the signs of KCDS?

Conjunctival hyperaemia, pain, lustreless cornea, low STT readings. Conjunctivitis, mucopurulent discharge.


What is the main sty treatment therapy for KCS?

Tear replacement with lubrithal gel, vislube, optixcare or lacrilube if let alone for any length of time. Tear stimulation with cyclosporine ointment either in conjunction with tear replacement or alone BID. Tacrolimus can be tried is cyclosporine doesnt work.


What is ephipora?

Overflow of tears due to poor drainage.


What is the cause of pigmentary keratitis?

Seen in the limbus along with new blood vessels in response to a variety of chronic corneal insults damaging the ocular surface. It is most frequently seen in brachycephalic breeds, due to prominence of the globe, macropalpebral fissure, nasal folds, medial canthal trichiasis, medial canthal entropion - all of which disrupt the tear film. also seen in KCS, entropion, pannus etc.


What is pannus? (chornic superficial keratoconjunctivitis)

A chronic superficial vascular keratitis occuring mostly in gsd, a rough fleshy looking infiltarte of inflammatory tissue, pigment and vessels advances across the cornea from the ventro lateral llimbus. the corneal epithelium is intact, therefore does not stain with flueorescein and signs of discomfort are mild or absent.


What is age related corneal endothelial degeneration? why does this occur and what does it look like?

Bilateral, can be assymetrical, degenerative condition of the corneal endothelium, occurring as a senile change in old dogs. The loss of endothelial cells causes failure of the endothelial pump mechanism, resulting in the steamy blue appearance of stromal oedema.


What is the prognosis for a retrobulbar tumour?

primary, secondary and tumours arising from the adjacent structures - 90% are malignant with low long term survival rates.


What are the causes of corneal ulcers?

external trauma
hair/lash trauma - entropion and ectopic cilia
Infection - fehv in cat, bacterial colonisation secondary to trauma, rarely fungal.
Tear film abnormalities - acute dry eye
Exposure keratopathy.

Ectopic cilium should be suspected when the ulcer is dorsally located. Ulcers under the third eyelid should not be overlooked, check for a foreign body.
Exposure keratopathy refers to the central corneal damage resulting from inadequate protection of the cornea by the eyelids and third eyelid, which may be compounded by inadequacy of the pre ocular tear film. Seen in prominent globe with poor lid closure or facial nerve paralysis.


What does a descmetocoele look like?

If the ulcer extends through the full thickness of the stroma to decemets membrane, fluorescein staining of a descmetocoele produces a characteristic green halo of stain with a clear centre as descemet's membrane repels the stain.


What are uveal cysts?

They arise from the posterior surface of the iris or the ciliary body, usually spontaneously, but sometimes following uveitis, they often break free and move around the anterior chamber. they may rupture, leaving remnants on the corneal endothelium. Treatment is not usually necessary, the main concern being distinguishing them form intraocular melanoma. Iris cysts are spherical, not solid, Black labs predisposed.


What is the most common intraocular tumour in all species?

Anterior uveal melanoma. usually the appearance is of a heavily pigmented solid mass within the iris or the ciliary body. They are often unrecognised by the owner until the development of secondary glaucoma. Benign and grow slowly, unucleation is usually curative.


what is anterior uveitis?what are the signs of this?

Inflammation of the iris and ciliary body. pain can be intense. Pain, visual disturbance, red eye, corneal oedema, breakdown of blood aqueous barrier - aqueous flare. Miosis - constricted pupil which responds poorly to light due to direct aciton of prostaglandins and other inflammatory mediators on the pupillary sphincter muscle.
Swelling of the iris- it looks puffy with loss of detail. Reduced intraocular pressure - drainage of aqeuous via the uveoscleral pathway is increased resulting in ddecreased IOP.


what therapy is indicated for anterior uveitis?

Deal with cause
Reduce intra ocular inflammation and restore blood aqeuous barrier
achive moderate mydriasis and pain relief
monitor iOP in order to detect any econdary glaucoma.
Steroids or NSAIds may be given otpically or systemically. Topical corticosteroids should begin immediately if cornea is intact.
Topical NSAIDS may be used i the cornea is ulcerated although may slow cornea re epithelisation.
Systemic steroids are indicated when the inflammation is severe and involves the posterior segment.
Atropine dilates the pupil, reducing the risk of extensive posterior synechiae formation. Give frequently in initial stages as much less effective in an inflamed eye.


what is the normal intraocular pressure for dogs and cats?

Dogs 16.8+/-4.0mmhg
Cat 20.3 +/- 5.5mmHg


What are the signs of acute glaucoma?

Pain:lethargy, avoidance behaviour
visual loss - may be unilateral so go unnoticed
Episcleral congestion
Corneal oedema
Moderately dilated pupil, poorly responsive to light.
Elevated IOP.
IOP measurement should be performed in every patient with unexplained red eye, ocular pain or visual loss.


Why does haemoglobinaemia and haemoglobinuria occur during haemolytic anaemia?

Intravascular haemolysis releases haemoglobin directly into the circulation. Haemoglobin binds avidly to plasma haptoglobin, which prevents the haemoglobin from spilling into the urine. Massive release of haemoglobin during acute severe intravascular haemolysis overwhelms haptoglobin binding, leading to haemoglobinaemia and haemoglobinuria.


What conditions lead to a secondary glaucoma?

Primary lens luxation
intraocular neoplasia
intraocular haemorrhage
retinal detachment
pigmentary glaucoma of the cairn terrier.


What treatment should be instigated in glaucoma?

Prostaglandin analogues - cause miosus and should be avoided in glaucoma secondary to uveitis/anterior lens luxation. usedd to treat acute primary glaucoma.

Osmotic diuretics - only used in emergency situation, contract the vitreous and will keep IOP down for several hours.

Carbonic anhydrase inhibitors - reduce aqueous production by up to 40% by reducing the amount produced by active secretion. Acetalozamide given systemically, side effects common so rarely used, better to give brinzolamide or dorzolamide topically.

B blockers -small reduction in aqueous production by reducing blood flow through ciliary process.


What is the prognosis for a retrobulbar tumour?

primary, secondary and tumours ariing from the adjacent structures - 90% are malignant with low long term survival rates.


How can SARD be distinguished from retrobulbar optic neuritis?

Electroretinography - ERG is present in optic neuritis, flat line in SARD. Assessing the pupillary and dazzle light reflezes using red abd blue light of specific wavelengths can also be used to distinguish conditions of the outer retina such as SARD form optic neuritis, as PLR and dazzle reflexes may persist when the blue light is used in SARD patients.


Why may bilateral prominence of the third eyelid occur in the cat?

Frequently observed in association with systemic disease, particularly diarrhoea,


What does chalmydophila felis cause?

primarily causes conjunctivitis without respiratory infection in all ages of ccats. it does not cause corneal ulceration.


What signs does feline herpes have?

Conjunctivitis and ulceration, usually 'cat flu' in young cats, in older cats - recrudescence of laterent infection can cause refractory ulcers, stromal keratitis or chornic conjunctivitis. corneal sequestrum formation and KCS quite common.


What is corneal sequestrum?what breed is this seen in?

Only seen int he cat, persians predisposed. clinical signs - a black plaque extruding through the corneal epithelium. Best treated by keratectomy. a conjunctival pedicle graft may be useful. sometimes no discomfort, the lesion appearing as tan coloured stromal discolouration - may not need treated.


A 8-year old Siamese cat presents to you with a single 2 cm skin mass on top of his head that is well circumscribed, hairless, dome-shaped and fixed to the overlying skin but freely movable from underlying fascia. The mass has been present for months and has been slowly growing. What is the most likely diagnosis?

The correct answer is basal cell tumor. This is the most common skin tumor in the cat (about 20% of all feline skin tumors). These tumors are usually hairless, dome-shaped, raised masses as described. They are most frequently found on the head, neck, and shoulders. They are almost always benign although histologically, they may have aggressive characteristics.


Why is fusidic acid not a great choice for prophylactic treatment of corneal ulcers?

It is not effective against pseudomonas.


What are the possible causes of haemolytic anaemia?

Immune mediated
Microangiopathic haemolysis (DIC, haemangiosarcoma)
Babesia infection
Heinz body haemolytic anaemia
Copper toxicity associated with hepatic necrosis
Zinc induced haemolytic anaemia
Severe hypophosphataemia
FelV associated haemolytic anaemia
Mycoplasma haemofelis.


What are the common causes of heinz body anaemias?

Toxicities due to paracetamol, onions, zinc and propylene glycol


What are the causes of a non regenerative anaemia?

Iron deficiency anaemia (chronic blood loss)
chronic renal failure
endogenous hyperoestrogenism
Felv associated non regnerative anaemia
Drug induced marrow failure e.g chemotherapeutics
IMHA of RBC precursors in bone marrow.
Anaemia of chronic disease
Lead poisoning
Chronic liver disease

Pure red cell aplasia
Aplastic anaemia
Haemopoietic neoplasia
Ineffective erythropoiesis


Why should cisplatin not be given to cats?

pulmonary edema typically occurs immediately with administration of the drug to cats. Cisplatin causes renal toxicity as well as nausea in dogs, but the fatal pulmonary edema is by far the most relevant side effect in cats.


Which clotting factors are vitamin K dependent?

II, VII IX and X


When does thrombocytopenia begin to show signs?

when platelet count drops below 40-50 x10^9, usual refereance range is 200-500


What is the best way of evaluating platelet function?

If platelet numbers are sufficient, platelet function can be evaluated via the buccal mucosal bleeding time. this should only be performed if the platelet count is not low eg below 50. the BMBt is the time elapsed until cessation of bleeding from a small standardised incision made in the buccal mucosa.


What is the activated clotting time?

Secondary haemostasis can be rapidly evaluated via the activated clotting time. the ACT is the time taken for fresh whole blood to clot in a glass tube containing a contact activator. A prolonged ACT indicates an abnormality affecting the intrinsic and common pathways of secondary homeostasis.


What is prothrombin and partial thromboplastin times?

Secondary haemostasis can be precisely evaluated by laboratories via analysis of prothrombin time, which tests extrinsic and common pathways and activated partial thromboplastin time, which tests intrinsic and common pathways.


How can measurement of excess fibrinolysis be detected?

high levels of FDPs, the end products of fibrin breakdown. D dimer tests for specific FDPS have also been used.


What are the possible causes of thrombocytopenia?

Aplastic anaemia, myeloproliferative disorders, megakaryocyte hypoplasia, neoplasia, chemotherapy, myelofibrosis, drugs.
Immune mediated thrombocytopaenia.
Consumptive coagulopathies e.g disseminated intravascular coagulation.


Which drus should be avoided/be prudent in animals with thrombocytopenia?

Penicillins aggravate clinical haemorrhage
Acepromazine, diazepam, ketamine propofol all impair platelet aggregation.
Famotidine has less of an effect on platelets than either cimetidine or ranitidine. These H1 and H2 blockers impair platelet aggregation.


What is von willi brands disease?

An autosomally inherited haemostatic disorder caused by a deficiency of von willebrand factor, a large glycoprotein that facilitates platelet function and is needed for primary haemostasis. Affected patients have a prolonged BMBT and decreased plasma levels of vwf. Desmopressin is sometimes used as a treatment.


How many throws should you do in a continuous pattern holding a coeliotomy closure?

7 throws start and finish


What is disseminated intravascular coagulation?

It is characterised by accelerated clotting leading to wide spread formation of microthrombi. The condition is often only recognised when uncontrolled thrombus formation leads to defective haemostasis and bleeding. widespread formation of microthrombi causes depletion of platelets and clotting factors and thereby predisposes to haemorrhage. Excessive quantities of FDP may be released as the fibrinolytic system attempts to break down the fibrin within microthrombi. FDP inhibit both paltelet function and various factors in the clotting cascade. DIC can be a complication of any severe systemic disease and is especially prevalent in haemangiosarcoma. DIC should be strongly suspected if haemostatic testing reveals thrombocytopenia, elevated FDP, decreased fibrinogen and prolonged BMBT, ACT


What is the treatment for canine immune mediated thrombocytopenia?

Glucocorticoid therapy. Decreases destruction of antibody coated cells byt he mononuclear phagocytic system. Dogs with IMT may respond to a single intravenous bolus of vincristine. Platepet rich plasma or fresh plasma may also be given although the increase in platelet numbers from plasma is usually minimal. Once thrombocytopenia has been in remission for 3-6 months therapy can be cautiously withdrawn.


Describe the different staging for multicentric lymphoma

I - a single node affected
II - two or more nodes affected in a regional area
III - generalised LN involvement
IV - Stage III plus liver and spleen involvement
Stage V - bone marrow and or non lymphoid organ involvement such as eye, CNs, lung.
a) all stage denotes no systemic clinical signs
b) all stage denotes presence of systemic clinical signs.


What side effect does doxorubicin have in cats?



What is the best treatment for low grade GI lymphoma?

oral prednisone and chlorambucil.


What is multiple myeloma?

malignant transofmarion and clonal expansion of a plasma cell . Typical features include hypergammaglobulinaemia - monoclonal gammopathy . Osteolytic bone lesions - lytic lesions often poorly defined or sharply punched out and may affect either the appendicular or axial skeleton. diagnosis of multiple myeloma requires; plasmacytosis of bone marrow, serum monoclonal gammoapthy, osteolytic lesions, bence jones proteinuria (two of the four).


What is the most common site of primary haemangiosarcoma?



What may haematology show in dogs with splenic haemangiosarcomas?

Frequently have coagulation abnormalities such as DIC or thrombocytopenia, Haematology may show polychromasia, hypochromasia, reticulocytosis, schisocytes, and nucleated RBCS on blood smears.


What is the main holding layer when closing a laparotomy?

External rectus sheath.


What is the difference between true and false hernias?

True hernias - enclosed in a peritoneal sac
False hernias - protrusions of organs outside a normal abdominal opening, not enclosed in a sac.


What muscle degenerates in a perineal hernia?

levator ani muscle - acquired degeneration of pelvic diaphragm.


What is a ranula?

A sublingual sialocoele


What are the signs of an oronasal fistula?

Chronic rhinitis
Nasal regurgitation of food
Aspiration pneumonia


What is the toxic dose of paracetamol?

200-600mg /kg in dogs
50-100 mg/kg in cats


Why are cats more susceptible to paracetamol toxicity?

There are low levels of glucuronyl transferase in the cat and thus reduced capacity for glucuronide conjugation, which means that biotransformation to Toxic metabolites occurs at a lower dose. Toxic effects are usually minimised by glucuronide conjugation of these metabolites.


What are the toxic effects of paracetamol in the cat?

the RBC is most susceptible to oxidative injury > haemoglobin is oxidised to methaemoglobin resulting in cyanosis and chocolate coloured mucous membranes. haemoglobin is also denatured resulting in heinz body anaemia. Signs include vomiting, ataxia, collapse and facial and pulmonary oedema.


What are the toxic effects of Paracetamol in the dog?

the liver is most susceptible to injury. Hepatocellular necrosis leads to the typical clinical signs of liver failure including depression,weakness, anorexia, vomiting and jaundice. Methaemoglobin/haemoglobinuria is also observed.


What is the treatment for paracetamol toxicity?

Induction of emesis or gastric lavage within 1-2 hours of ingestion, administration of activated charcoal, supplemental oxygen, IVFT, blood transfusion. Glutathione precursors are administered to replenish cellular glutathione, N acetylcystine or S adenosyl -methionine. Vitamin C and methylene blue can be used to reduce methaemoglobin to haemoglobin.


What are the clinical signs of NSAID toxicity?

Vomiting, depression, anorexia, diarrhoea, melena and PUPD. Various factors increase the risk - v young or old animals, hypoalbuminaemia, concurrent use of glucocorticoids, gastrointestinal perforation may also occur with animals presenting with peritonitis.


What is the treatment for ibuprofen toxicity?

IVFT, induce emesis/gastric lavage, activated charcola, misoprostol, h2 antagonists, proton pump inhibitors and sucralfate.


How does ethylene glycol cause toxicity? What are the symptoms?

EG itself causes vomiting due to gastrointestinal irritation and CNS depression, toxicity is caused by metabolism of EG to glycoaldehyde, glycolic acid and oxalate. Glycoaldehyde results in CNS depression, ataxia, stupor and seizures. Severe metabolic acidosis occurs as a result of glycolic acid accumulation. Glycoaldehyde results in CNS depression, ataxia, stupor and seizures. Severe metabolic acidosis occurs as a result of glycolic acid accumulation. Most of the metabolites are directly toxic to the renal tubular epithelium and formation of calcium oxalate crystals, contributes to anuric/oliguric renal failure.


How can diagnosis of EG poisoning be made?

High anion gap - metabolic acidosis, before the onset of ARF.
Renal damage, azotaemia, hhyperphosphataemia, hyperkalaemia, hypocalcaemia, and hyperlycaemia, isosthenuria, calcium oxalate crystalluria, renal ultrasonography 0 increased cortical echogenicity and medullary rim sign.


How is EG toxicity treated?

administration of drugs which inhibit alcohol dehydrogenase eg ethanol or 4-methylpyrazole. Thiamine and pyridoxine enhance metabolism of glycoxylic acid to non toxic metabolites. aggressive IVFT to maintain renal perfusion. mannitol to promote diuresis. bicarbonate therapy for metabolic acidosis.


What other toxins cause acute renal failure in dogs and cats?

Easter lily - cats
Raisin/grape/sultana - dogs


What are the clinical signs of metaldehyde poisoning?

It inhibits yamino-butyric acid (GABA). Clinical signs occur within 1-3 hours and incluce abdominal discomfort, salivation vomiting, tachycardia, tachypnoea, hyperaesthesia, hyperthermia, opisthotonus and convulsions.


What are the signs of permethrin toxicity in cats?

Permethrins affect sodium channels resulting in repetitive nerve stimulation and most commonly seen in excitatory neurological signs - tremors, seizures, although ataxia and depression may also be seen.


How does chocolate cause toxicity? How is it treated?

chocolate contains theobromine, a methylxanthine like caffeine and theophylline, which antagonises the effects of adenosine. Acute intoxication results in restlessness, panting,diuresis, vomiting and diarrhoea and may progress to give rise to CNS excitation and cardiac arrythmias. Supportive therapy with IVFT, muscle relaxants, anti arrhythmic drugs, beta blockers, may be required for supraventricular tachycardias.


What are the clinical signs of toxicity with organophsphates/carbamateS?

These are insecticides that exert their neurotoxicity by inibition of acetylcholinesterase which results in prolonged activity of acetylcholine at the neuromuscular junction. nicotinic signs include muscle tremors, generalised muscle tetany followed by weakness due to the inability of the membranes to repolarise adequately. CNS signs include anxiety, hyperactivity, tonic clonic seizures to severe CNS depression. In addition, muscarinic signs of salivation, lacrimation, urination and defecation are usually observed prior to the onset of nicotinic signs. Bradycardia, dyspnoea and miosis may also occur.


which breed are most sensitive to toxicity with avermectins and why? what is the treatment of this?

Avermectins cause CNS depression due to enhanced GABA activity. collie breeds appear to be more sensitive due to an inability to expel these compounds fmor the CSF. clinical signs include bradycardia, respiratory depression, CNS deoression and coma. Reduce further absiorption, induce emesis or perform gastric lavage if within 1-2 hours of ingestion. Administer activated charcoal. IVFT, maintenance of body temperature, respiratory support.


What are the clinical signs of anticoagulant rodenticide toxicity? How do these work?

Anticoagulants include warfarin, bromadiolone, and difenacoum. They inhibit vitmain K epoxide reductase and prevent recycling of vitamin K in the liver. The result is that synthesis of vitamin K dependent coagulation factors II, VII, IX, X is impaired and these factors become depleted resulting in coagluopathy. there may be a lag of 3-5 days between ingestion of toxin and clinical signs. Common presentation includes epistaxis, haemoptysis, dyspnoea due to haemorrhage, haematoma, pallor of mucous membranes. Diagnsis based on prolongation of both prothrombin time, and activated partial thromboplastin time, as both the intrinsic and extrinsic coagulation factors are affected.


What is the treatment for rodenticide toxicity?

Vitamin K1 therapy subcut followed by oral administration, continued for as long as 4 weeks. PT should be measured 36-48 and 72 hours after cessation of therapy. due to short half life of factor VII 6 hours, the PT is the first parameter to become prologned if duration of therapy is not sufficient. Treatment should then be continued for a further 7 days then coagulation re assessed.


How can fungal rhinitis be diagnosed?

Impression smear of nasal discharge for C neoformans + Positive LCAT. Histopathology and fungal culture of nasal biopsy for aspergillus. supportive features would include destruction of nasal turbinates on radiography/ct and positive aspergillus serollogy. tx- topical infusion of clotrimazole via nasal catheters, systemic itraconazole.


What type of breeds is tracheal collapse more common in?

toy breeds. other anatomical abnormalities such as hypoplastic trachea, laryngeal collapse, extended soft palate etc more common in toy and brachycephalic dogs.


What breeds are chronic bronchitis and chronic pulmonary interstitial disease more common in?

Terrier breeds.


you have been presented with a middle age yorkshire terrier which has a chronic cough, what is your top differential?

Tracheal collapse


You are presented with a 8 year old WHWT with dyspnoea, exercise intolerance and coughing with obvious inspiratory crackles. what is your top differential?

Idiopathic pulmonary fibrosis.


You are presented with a 10 year old labrador with intermittent exercise intolerance with stridor, typically associated with excitement and dysphonia. what is your top differential?

Laryngeal paralysis.


When do crackles occur?

inspiratory - due to reopening of airways that have closed during expiration.


what are wheezes?

High pitched sounds that can be inspiratory or expiratory and are due to narrowing of the bronchial lumen. common in feline asthma.


What are rhonchi?

Low pitched sounds due to high airflow velocity through the larger airways, can be inspiratory or expiratory and can be normal if exercise or excitement associated. In disease they can arise because of anything necessitating increased respiratory effort with pneumonia and pulmonary oedema being a good example.


Describe the typical presentation of tracheal collapse. How can this be diagnosed and treated?

Small breeds of dogs, toy breeds, especially yorkshire terrier.
Lack of structural integrity increases the collapsibility of the trachea.
Clinical signs mainly apparent in middle age, with severe tracheal abnormality causing problems in young dogs. Coughing (goose-honk or seal bark sond) associated with excitement, exercise and lead pulling easily elicited on gentle tracheal compression. Isnpiratory dyspnoea occurs if extra thoracic trachea is prone to colapse while expiratory dyspnoea is caused by intra thoracic tracheal collapse. cyanosis and syncope during particularly severe attacks. radiography might demonstrate collapse of the trachea, primarily at the thoracic inlet and cranial mediastinal area. Bronchoscopy demonstrates dorsoventral flattening of the trachea and redundancy of the dorsal membrane. Treatment is by controlling obesity, use of a harness, avoidance of excessive exercise and stressful situations. Surgical correction or intra lumenal stenting of the collapse can be of value and may be the only course of action in severely affected animals.


What is the most common cause of coughing in dogs? How can this be treated?

Acute tracheobronchitis - infective material is transmitted by direct contact, as aerosolised infective respiratory secretions and via fomites. Agents include bordetella bronchiseptica, parainfluenza III, canine distemper virus, canine adenovirus II and canine herpes virus. There is harsh non productive coughing exacerbated by exercise or excitement, mild pyrexia, lethargy and inappetance and naso ocular discharge. Condition is usually self limiting with the clinical signs persisting for up to three weeks. Tetracyclines and potentiated sulphonamides are usually effective in reducing the duration of clinical signs but antibacterial therapy is not necessarily required. In a small proportion of cases, residual coughing may be present.


How does chronic bordetellosis infection occur? how can it be treated?

A sporadically occuring condition, recognised primarily in dogs that have had kennel cough. There appears to be a heightened cough reflex, resulting in harsh non productive coughing. clinical signs usually appear severeal weeks after apparent resolution of kennel cough with no other clinical abnormalities. Bronchoscopy and bronchial cytology are normal in the majority of dogs. Radiography shows a mild to moderate increase in bronchial markings. No specific therapy is recommended, spontaneous resolution over a period of months may occur, the use of anti tussives may help, a harness rather than a dog collar may help. If bordetella positive wash then a 3 week course of doxycyline should be tried. Dogs can continue to cough for several years.


What is chronic bronchitis?

A mucus hypersecretory disorder affecting the bronchi. Excessive mucus production is a reaction to airway inflammation and a cause of further bronchopulmonary problems. Recurrent bouts of bacterial bronchitis and bronchopneumonia causes irreversible damage leading to alveolar fibrosis and respiratory failure. On radiography a prominent bronchial pattern is often present. Secondary cardiac changes may also be noted. Anti tussives should not be used under any circumstances. Progressive, irreversible, prognosis poor


What is bronchomalacia?

A loss of bronchial wall rigidity, elderly dogs with chronic cough, often seen with chronic bronchitis, no treatment. Similar clinical presentation as chronic bronchitis. Misshapen larger airways that easily collapse during expiration.


What is felne asthma syndrome? how is this diagnoseD?

Probably a type I immediate type hypersensitivity reaction to inhaled allergens. clinical signs can vary from mild coughing to severe dyspnoea, cyanosis and death. paroxysmal coughing, wheezing usually associated with the coughing attacks. Dyspnoea and tachypnoea with head extension and open mouth breathing. Haematology - circulating eosinophilia may be found and is highly supportive of a diagnosis. radiography findings vary from mild bronchial markings to severe interstitial changes with right middle lobe collapse/consolidation. The majority of cats are controlled with oral low dose alternate day prednisolone. nebulized glucocorticoids and B adrenoceptor agonists are used by some.


How do airway and lung parasites affect dogs and cats? how are these treated?

Crenosoma vulpis - dog
Aleurostrongylus abstrusus - cat
Angiostrongylus vasorum
Reactive tracheitis, bronchitis and alveolitis results giving the clinical signs of paroxysmal episodes of a harsh cough, dyspnoea if airways are occluded or infection is widespread. Radiography usually normal. reactive nodules may be seen at the carina. interstitial pattern if significant lung eosinophil infiltration. Grey brown to white ish reactive nodules visible at the carina on bronchoscopy. Treatment - benzimidazole anthelmintics are effective e.g fenbendazole and spot ons eg advocate.


What are the typical signs of an airway foreign body?

Acute onset coughing that can be continuous, harsh and very distressful, subsides over subsequent days and becomes chronic. pronounced halitosis will develop over the following weeks to months. signs of acute bronchopneumonia or pleural effusion can develop in complicated cases. Bronchoscopy allows identification of the foriegn body, its eact location and retrieval.


How does pneumonia occur? what will be seen on radiography? what are the clinical signs?

An inflammatory disease of the lung parenchyma including the interstitium, alveolar spaces and the msaller bronchi, bronchioles and respiratory bronchioles are grouped together as pneumonia. viral and primary bacterial agents causes are not that important in the aetiology. Secondary bacterial infection is common and typical agents include pasteurella, klebsiella and proteus. acitnomyces and nocardia spp occasionally involved. often secondary to other diseases such as chronic bronchitis, inhalation of foreign material, systemic illness. Haematology that shows the presence of a leucocytosis with a neutrophilia and left shift is suggestive of acut ebacterial bronchopneumonia. An alveolar pattern on radiographs will be seen with distinctive air bronchograms - attributed to bronchopneumonia. On bronchoscopy - mucopurulent material in the airways. Anti tussives are contraindicated .empirical antibacterial therapy is acceptable with broad spectrum. Mucolysis using nebulised solutions and steam vapour can be useful.


What is pulmonary infiltration with eosinophils? what are the clinical signs and treatment for this?

Grou of espiratory isease, eosinoophil is the predominant cell type, PIE is believed to involve a hypersensitivity reaction to inhaled allergens or migrating ascarid parasites, clinical signs vary, affected dogs are usually otherwise clinically normal, coughing is seen with tachypnoea and dyspnoea, marked circulating eosinophilia may be present, circulating basophilia more significant. Moredate interstital pattern common on radiographs. The treatment is glucocorticoids. Prognosis can vary with some dogs responding to a single treatment and others requiring chronic treatment due to recurrence.


What is idiopathic pulmonary fibrosis? How is this diagnosed and treated?

Terrier breeds, particularly the west highland white and cairn terrier are affected, lung fibrosis, gradual onset and progressive deterioration, coughing, tachypnoea, dyspnoea and exercise intolerance, cyanosis, marked crackles are audible on chest auscultation, CT is the best method of diagnosis with characteristic changes including ground glass appearance, sub pleural fibrosis, parenchymal bands, traction bronchiectasis and occasionally honey comb appearance to lung. Glucocorticoid therapy is beneficial in some cases and some dogs seem to benefit from additional bronchodilator therapy. sildenafil and pimobendan for those with pulmonary hypertension gives symptomatic relief.


What is the most common pulmonary primary neoplasm?

Adenocarcinoma. on rads - commonly a well delineated mass. alleviation of clinical signs with glucocorticoids for several weeks to months. Surgical removal can be attempted if localised to single lobes. Terminal disease.


How do pleural effusions occur? what are the common clinical signs? how can this be diagnosed?

Pleural effusion restricts lung expansion resulting in varying degrees of tachypnoea, dyspnoea and exercise intolerance. With severe effusions cyanosis may develop. Pyrexia may be present with pyothorax. Muffling of respiratory and cardiac sounds in alteration in chest percussion can be found. Thoracocentesis sampling form pleural space allows identification of the effusion type and culture of the infective organisms. biochemistry identifies hypoalbuminaemia sufficient to cause transudate as well as evidence of hepatic dysfunction. Serum triglyceride levels can be compared to levels in effusions.


What are the typical radiographic findings with pleural effusion?

A homogenous ground glass appearance, pleural fluid lines, lung lobe border delineation, lung lobe compression.


What are the possible causes of a transudate pleural effusion?

Hypoalbuminaemia, congestive heart failure


What are the possible causes of a modified transudate pleural effusion?

Increased numbers of cells and protein, yellow/pink - cardiac disease, hypoalbuminaemia, obstruction of lymphatic drainage, inflammatory, reaction to neoplasia, herniation of abdominal cnotents.


What are the possible causes of a exudate pleural effusion?

Inflammation, infection, neoplasia


What are the possible reasons for chylothorax?

Trauma, neoplasia, infections, idiopathic, congenital, congestive heart failure.


How should pyothorax be treated?

Treat vigorously with intermittent or continuous chest drainage. this allows chest lavage with warmed normal saline. long term antibacterial therapy on the basis of culture and sensitivity testing. penicillins, other B lactam agents, clindamycin, potentiated sulphonamides for dealing with anaerobic infections.


How can chylothorax be managed?

Dietary control of fat intake and surgical ligation of the thoracic duct. treatment of underlying infections and neoplastic diseases. benzopyrones in the treatment of chylothorax in dogs may be of potential benefit but their efficacy is still being assessed and no definite recommendation on their use is available.


What are the typical symptoms seen in mediastinal disease?

Coughing, dyspnoea, dysphagia, regurgitation, neck/forelimb oedema, ascites and hindlimb oedema, chylothorax, horners syndrome, laryngeal dysfunction.


What are the typical causes of pneumomediastinum?

Tracheal or oesophageal rupture, iatrogenic puncture of trachea or bronchi, idiopathic pneumomediastinum is found although it may be assocaited with forceful respiratory manoevres such as coughing, deep neck wounds with air migrating along the neck/muscle facial planes.


What is demodex gatoi?

Demodex gatoi and Demodex cati are the two demodex mites seen in cats. Demodex gatoi is the more short and stubby mite which lives superficially and Demodex cati is the long slender mite which lives in the hair follicles. Demodex gatoi is considered contagious to other cats and causes pruritus.


What do B2 agonists do?

They are the most effective bronchodilators - they relax airway smooth muscle, some of them may also modulate mediator release from mast cells and TNF-a release from monocytes. B receptors also stimulate airway mucus secretion. Specific b2 agonsts include short acting agents such as salbutamol, terbutaline and clenbuterol. Maximum effects occur within minutes. Duration of action is 4-6h.


What are methylxathines?

also bronchodilators - reduce cAMP breakdown via PDE inhibition. They decrease effort associated with breathing. this class includes caffeiene, theobromine, theophylline.


What mucolytics can be used to treat chronic bronchitis? how do they work?

They break down thick dry mucous, they may act on mucus secreting cells or on mucus directly. modifiers of mucus synthesi include bromhexine (bisolvon) and dembrexine (sputulosin) and are often used to treat chronic bronchitis. they reduce the viscosity of secreted mucus and possibly by increasing lysosomal breakdown of mucopolysacharide within the gland cell.


How do anti tussives work?

They can act centrally or peripherally. centrally acting drugs include narcotic opiate analgesics cdeine, hydrocodone, butorphanol, and non narcotic opioids dextromethoprhan, diphenyoxylate. Their use is limted to those cases where coughing is of little value and cannot b controlled by other means and is causing significant discomfort to the dog. Care should be exercised in their use when coughing is of benefit to the patient eg chronic bronchitis and pneumonia.


Which antibiotics are lkely to be effective in resrpiatory infections?

Majority are gram negative aerobes so - fluoroquinolones. Pradofloxacin has enhanced anti gram positive activity. A typical approach would be any three of clindamycin, a cephalosporin, potentiated sulphonamides and an early generation fluoroquinolone. Amoxicillin clavulanate is limited on its penetration into infected lung. If mycoplasma suspected then use doxycyline, Gentamycin can also be considered for highly resistant pseudomonas infection but parenteral fluoroquinolones or ticarcilin are more feasible. tx for a minimum of 4 weeks in bronchopneumonia.


Which drugs can be used to treat pulmonary hypertension?

Sildenafil and pimobendan - likely acting as PDE5 inhibitors.