VIN Class 4 - Canine Info

Question 1

Topic: Canine Hypothyroidism
1. Hypothyroidism is common in dogs of what age? It can also be?
2. What is the most common etiology?
3. What is the most common cause of misdiagnosis?
4. How do you diagnosis hypothyroidism?

Answer 1

1. Most common in older dogs but can also be congenital (cretinism - rare).
2. Hypothyroidism most commonly occurs in dogs due to lymphocytic thyroiditis.
3. The most common cause of misdiagnosis is suppressed hypothalamic-pituitary stimulation of the thyroid due to illness (euthyroid sick syndrome).
4. The thyroid gland synthesizes the thyroid hormones thyroxine (T4) and triiodothyronine
   (T3) which incorporate iodine. The hormones are responsible for a wide range of physiologic effects, but most importantly they increase metabolic rate, oxygen consumption, heart rate, erythropoiesis, and catecholamine response. They have catabolic effects on muscle and adipose tissue.

Question 2

Topic: Canine Hypothyroidism Cont.
5. What are the main clinical signs of canine hypothyroidism?
6. How is this disease diagnosed? What is the preferred screening test? What is the confirmatory test? ***
7. How is this disease treated?

Answer 2

5. Weight gain, obesity, lethargy, alopecia (often bilaterally symmetric over the lateral trunk, tail, and ventral thorax)
6. A. Bloodwork - Mild non-regenerative anemia, Hypercholesterolemia
   B. Serum total T4 level is the preferred screening test.
   C. Dogs with low T4 levels may be hypothyroid but this should be confirmed by:
   - Treat any identified underlying conditions
   - cTSH and free T4 by equilibrium dialysis levels
   - if the dog is hypothyroid the cTSH will be elevated and the free T4 will be low.
   - TSH stimulation test: Hypothyroid dogs should have low T4, even after TSH stimulation
   - Trial of T4 replacement therapy and assess response
7. Levothyroxine - Optimal dosing varies among dogs and T4 levels should be evaluated after beginning therapy and while treatment is maintained. The dose should be calculated based on the dog’s ideal body weight.

Question 3

Topic: Canine Hypoadrenocorticism
1. What is the cause of hypoadrenocorticism? Explain how this affects the body.
2. Describe the signalment and clinical signs seen in patients.
3. What diagnostics should you run? What would you see? **
4. What is the diagnostic test of choice?
5. What is the acute vs chronic treatment? **

Answer 3

1. Inadequate adrenal production of glucocorticoids and mineralocorticoids, most commonly from idiopathic adrenocortical atrophy. Glucocorticoids are needed by nearly every organ in the body for homeostatic function and glucose regulation. Mineralocorticoid deficiency leads to an inability to retain sodium or to excrete potassium and hydrogen resulting in hypotonic dehydration, hyperkalemia and metabolic acidosis.
2. Often middle aged (3-7 years, mean 4 years old), 70% females. Breed predilections: Standard Poodles (black), Portuguese Water Dogs, Great Danes, Rottweilers, West
   Highland White Terriers, Wheaton Terriers. Acute - Hypovolemic shock with weakness and vomiting (maybe hematemesis). Chronic - May see worsening of signs at stressful periods. Polyuria, polydypsia. Nonspecific and
   often mistaken for renal disease, GI disease or pancreatitis.
3. A. Hyperkalemia, hyponatremia (Na: K ratio of < 27) hypochloremia, hypercalcemia, hypoglycemia
   B. Low specific gravity (<1.030)
   C. Bradycardia and ECG changes consistent with hyperkalemia (tall tented T waves, diminished to absent P waves, prolonged P-R interval, wide QRS complexes)
4. Measure serum cortisol before and after administration of ACTH gel or synthetic ACTH.
   a. Normal dogs generally have post-stimulation cortisol levels >10 ug/dl. Post stimulation levels <2 ug/dl is considered diagnostic and most patients are <1 ug/dl. Administration of any steroid other than dexamethasone will invalidate this test.
5. A. Restore blood volume: Rapid administration of fluids. 60-90 ml/kg. This will
   restore perfusion to organs including the kidneys and reduce hyperkalemia through increased GFR and dilutional effects. Classically, fluid of choice is 0.9% NaCl.
   B. Treat hyperkalemia if necessary: While fluid therapy is often sufficient to reverse hyperkalemia, if cardiac abnormalities are significant, temporary cardio-protection with calcium gluconate may be necessary in addition to glucose, insulin or bicarbonate to promote intracellular shift of potassium.
   C. Intravenous glucocorticoids: Dexamethasone SP is often preferred as it will not interfere with diagnostic tests.
   D. Begin maintenance therapy of corticosteroids and mineralocorticoids (see below).

E. Lifetime corticosteroid maintenance: Prednisone or prednisolone
F. Lifetime mineralocorticoid supplementation: Options include oral fludrocortisone (given daily) or
injectable DOCP (desoxycorticosterone pivilate) every 3-4 weeks.

Question 4

Topic: Hyperadrenocorticism (Cushing’s Syndrome)
1. What causes this disease?
2. What are the clinical signs?
3. What diagnostic tests should you run? What do you see?

Answer 4

1. Signs of Cushing’s disease can come from ACTH secreting pituitary tumors, cortisol secreting adrenal tumors, or iatrogenic steroid administration.
2. PU/PD, Panting, Polyphagia, Pendulous abdomen, Pyoderma and thin skin, Pigmentation and symmetrical alopecia
3. A. Stress leukogram – neutrophilia, lymphopenia
   B. Elevated ALP (alkaline phosphatase)
   C. Hyposthenuria (USG < 1.010
   D. Low Dose Dexamethasone Suppression Test: Measure plasma cortisol before and at 4 and 8 hours after IV dexamethasone (0.01mg/kg). 90% of dogs with Cushing’s will have 8 hour cortisol levels >1.4 ug/dl. This test can also be used to help differentiate PDH from AT because for PDH, you often see some reduction (<50% basal value) of cortisol at 4 hours but not for AT.
   E. ACTH Stimulation Test: Measure cortisol levels before and after administration of ACTH. Was considered the test of choice for diagnosis for many years although this is no longer true. Is still the most commonly used test for monitoring therapy for hyperadrenocorticism.
   F. AUS
   G. Urine Cortisol
   H. Endogenous ACTH
   I. High-dose Dex
   J. 170-hydroxyprogesterone - atypical cushing’s

Question 5

Topic: Hyperadrenocorticism (Cushing’s Syndrome)
5. Treatment

Answer 5

5. A. Mitotane - o,p’DDD. Causes adrenocorticolysis - Essentially a chemical partial adrenalectomy. Induction and maintenance therapy must be monitored by ACTH stimulation tests to avoid causing hypoadrenocorticism.
   B. Trilostane - An oral steroid analogue that inhibits cortisol and aldosterone synthesis.
   Requires similar monitoring.
   C. Selegiline (Anipryl, L-Deprenyl) - Not currently recommended for the dog.
   D. Ketoconazole - May be associated with high occurrences of side effects.
   E. Surgery - Adrenalectomy or hypophysectomy are rarely performed options in North America.

Question 6

Topic: Diabetes Mellitus in Canids
1. What is the etiology of DM ?
2. Name the key clinical signs in a healthy diabetic patient.
3. Name the key clinical signs in a diabetic ketoacidosis patient.
4. What diagnostics can you run on a DM patient? What will you see?
5. How is a healthy DM treated?
6. How is a DKA patient treated?

Answer 6

1. Inadequate insulin production or insulin resistance.
2. The key clinical signs in a healthy diabetic patient are:
   - PU/PD
   - Polyphagia
   - Weight loss
   - Recurrent infections
   - Cataracts in dogs
3. The key clinical signs in a DKA patient are:
   - Anorexia
   - Vomiting
   - Weakness
   - BG > 500
   - Severe metabolic acidosis
4. • BG; Will see hyperglycemia (usually > 300)
   • USG: Will see Glucosuria +/- ketonuria
   • BW: Metabolic acidosis, elevated liver enzymes and cholesterol
5. Healthy DM:
   - Insulin: Nearly all intermediate and long-acting insulins (Vetsulin, PZI, NPH, lente, ultralente, Glargine) are acceptable for managing the healthy diabetic. Insulin therapy should be monitored by blood glucose curves.
   - Diet: High fiber, moderate fat
   - Oral Hypoglycemics such as Glipizide (Glucotrol) - the most widely used oral hypoglycemic. Efficacy is controversial.
6. DKA:
   - Aggressive IV Fluids – 0.9% saline with potassium and phosphate supplementation
   - Regular insulin: Regular insulin is the fast-acting insulin of choice for severe DKA. It can be given intermittently (q 6-8 hrs) or by continuous IV infusion. With either, frequent blood glucose monitoring and insulin dose adjustment is necessary to achieve gradual decline in blood glucose level.
   - Bicarbonate Therapy - if metabolic acidosis is severe and/or not improving with IV fluids.
   - Identify and address any concurrent infections or diseases.

Question 7

List the duration of action of each insulin type from shorted to longest for both canine and feline DM patients:

Answer 7

Regular < NPH < Lente < PZI < Glargine < Detemir

Question 8

Topic: Canine Parvovirus
1. Canine Parvovirus is a common cause of ?
2. What is the pathophysiology of canine parvovirus?
3. List the clinical signs.
4. How is this condition diagnosed? What is the confirmatory test?
5. How is this disease treated?
6. How can this disease be prevented?

Answer 8

1. Enteritis in young, unvaccinated dogs.
2. CPV-2 is highly contagious, spread by fecal-oral route. Virus is extremely long lived and resistant. Small amounts of fecal contamination of a fomite can be a source of transmission. The virus destroys rapidly dividing cells in intestinal crypts causing secondary villous atrophy.
3. • Leukopenia, fever
   • Severe, often bloody, diarrhea
   • Vomiting, loss of appetite, lethargy, dehydration
4. • Diagnosis is based on history, c/s, and lab work (leukopenia)
   • Confirmed with fecal parvovirus ELISA test
5. No specific tx; Just supportive care
   - IV Fluid Therapy- Correct initial fluid and electrolyte deficits and then account for ongoing losses and/or lack of intake.
   - Systemic antibiotics- IV broad spectrum coverage- (i.e. Amikacin and potentiated clavulanic acid or
   enrofloxacin and ampicillin/ cefazolin/ metronidazole). Beware of antibiotics that should not be used in young, growing animals!!!
   - Anti-emetics- i.e. Metoclopramide, chlorpromazine, maropitant (Cerenia).
   - Gastric protectants- i.e. Ranitidine, omeprazole, sucralfate.
   - Other considerations- anti-inflammatories, rG-CSF, nutrition, anti-parasitics.
6. Vaccination, Careful hygiene, Isolation of ill animals, Disinfection with bleach

Question 9

Foreign Body

Question 10

Pyometra

Question 11

Congestive Heart Failure

Question 12

Topic: Dilated Cardiomyopathy
1. What type of disease is DCM? What is it characterized by?
2. What breeds are predisposed to DCM?
3. What clinical signs are seen in cases of DCM?
4. How is DCM diagnosed?
5. How is it treated?

Answer 12

1. DCM is a primary myocardial disease characterized by cardiac enlargement and impaired systolic function.
2. Doberman, Irish Wolfhound, Great Dane, St. Bernard, Newfoundland, Leonberger, Boxer, Giant Schnauzer, Cocker Spaniel, Flat Coat Retriever.
3. Early signs:
   - Fainting, lethargy, exercise intolerance.
   - Many dogs are asymptomatic until they suddenly have symptoms associated with heart failure; onset of symptoms may be extremely rapid (a few days).
   Signs of heart failure:
   - Respiratory distress from left-sided congestive heart failure.
   - Abdominal distention from ascites from right-sided congestive heart failure
4. Echocardiogram - systolic cardiac dysfunction (poor contractility and shortening fraction)
5. • Subclinical dogs: ACE inhibitors and/or pimobendan for dogs with early stage cardiac dilatation.
   • For dogs with arrhythmias: ventricular tachycardia (especially in Boxers and Dobermans), options include sotalol, amiodarone, mexilitine, and very low dose atenolol.

Question 13

Topic: Familial Arrhthmic Cardiomyopathy
1. AKA?
2. What type of disease is this? What breed is predisposed?
3. What is the major clinical sign?
4. How is this disease diagnosed?
5. How is this disease treated?

Answer 13

1. Arrhythmogenic Right Ventricular Cardiomyopathy
2. Autosomal dominant, primarily boxer dogs
3. Syncope; Can cause sudden death even in young dogs.
4. Diagnosis typically requires a 24 hour Holter monitor to assess the severity and response to
   treatment because a brief ECG may dramatically overestimate or underestimate the frequency of
   VPCs due to their intermittent nature.
5. A. In asymptomatic dogs with VPCs: While strict diagnostic criteria do not exist, >100 VPCs per 24 hours or runs of couplets, triplets, or ventricular tachycardia is consistent with disease and >1000 VPCs per 24 hours, runs of ventricular tachycardia, or evidence of R on T warrant treatment.
   B. In symptomatic dogs (dogs with syncope)
   i. Two options are sotalol or the combination of mexilitine and atenolol
6. If a poor response is seen with one option, the other may be more effective
   C. In dogs with systolic dysfunction and heart failure, they should be treated as dogs with DCM. Also, some cardiologists advocate supplementing L-carnitine.

Question 14

Mitral Valve Disease

Question 15

Topic: Toxocara spp.

1. What are the clinical signs associated with this parasite?
2. Describe the pathogenesis
3. Are they zoonotic?

Answer 15

1. Gastrointestinal symptoms such as vomiting or diarrhea
   - Sometimes, worms are seen in feces or vomit
   - Puppies/kittens are usually more affected and can have more severe symptoms such as difficulty gaining weight, unthriftiness and pot-bellied appearance
   - Heavy Toxocara infections can be life threatening
2. Following acquisition, larvae of Toxocara spp. migrate through the liver and lungs, are carried up the mucociliary apparatus, and then are swallowed to develop in the small intestine.
3. High zoonotic potential; T. canis in particular is associated with visceral larval migrans in humans

Question 16

Topic: Toxocara canis
1. What is the domestic small animal DEFINITIVE host?
2. Where are the worms located?
3. List the routes of transmission. Which of these is the most common?
4. How is it diagnosed?
5. How is it treated?

Answer 16

1. dogs
2. small intestine
3. • Transplacental/Transuterine (most common)
   • Ingestion of eggs with L3 larvae
   • Ingestion of paratenic host
   • Transmammary
4. fecal flotation
5. Fenbendazole, Milbemycin oxime, Moxidectin, Pyrantel

Question 17

Topic: Toxocara leonina
1. What is the domestic small animal DEFINITIVE host?
2. Where are the worms located?
3. List the routes of transmission. Which of these is the most common?
4. How is it diagnosed?
5. What is different about this species of Toxocara?
6. How is it treated?

Answer 17

1. cats and dogs
2. small intestine
3. • Ingestion of eggs infected with L3 larvae
   • Ingestion of paratenic host
4. fecal flotation
5. Unlike other Toxocara species, migration outside the gastrointestinal tract doesn’t occur
6. Fenbendazole, Milbemycin oxime, Moxidectin, Pyrantel

Question 18

Topic: Ancyclostoma spp.
1. What are the clinical signs associated with this parasite?
2. Are they zoonotic?

Answer 18

1. Gastrointestinal symptoms such as diarrhea
   - More severe possible clinical signs include anemia, lethargy, melena and weight loss
   - Puppies/kittens are usually most severely affected
   - Heavy Ancylostoma infections can be life threatening
2. Ancylostoma spp are associated with high zoonotic potential. Associated with cutaneous larval migrans in humans

Question 19

Topic: Ancyclostoma caninum
1. What is the domestic small animal DEFINITIVE host?
2. Where are the worms located?
3. List the routes of transmission. Which of these is the most common?
4. How is it diagnosed?
5. How is it treated?

Answer 19

1. dogs
2. small intestine
3. a. Transmammary (important route)
   b. Ingestion of L3 larvae
   c. Ingestion of paratenic hosts
   d. Transplacental infection
   e. Third stage larva penetrate skin
4. fecal flotation
5. For adult A. caninum:
   - Fenbendazole
   - Milbemycin oxime
   - Moxidectin
   - Pyrantel pamoate

For L4 A. caninum:
Moxidectin

Question 20

Topic: Ancyclostoma braziliense
1. What is the domestic small animal DEFINITIVE host?
2. Where are the worms located?
3. List the routes of transmission.
4. How is it diagnosed?
5. How is it treated?

Answer 20

1. dogs and cats
2. small intestine
3. a. Oral ingestion of 3rd stage larvae
   b. Larval penetration of the skin
   c. Ingestion of paratenic hosts
   d. Transmammary/transplacental
4. fecal flotation
5. For adult A. braziliense in dogs: Pyrantel pamoate

Question 21

Topic. Trichuris vulpis
1. What is the domestic small animal DEFINITIVE host? ***
2. Where are the worms located?
3. List the routes of transmission.
4. How is it diagnosed?
5. How is it treated?

Answer 21

1. dogs
2. cecum
3. Ingestion of infective L2 stage eggs
4. fecal flotation with centrifugation, high specific gravity
   - Note: Due to intermittent shedding, density and small number of eggs, may be difficult to diagnose on fecal float
5. Single dose: Febantel + Pyrantel; Pamoate + Praziquantel (Drontal Plus)R; Fenbendazole for three days, repeated monthly for 3 months

Question 22

Topic: Trichuris spp.
1. What are the clinical signs associated with this parasite? What may they cause?
2. What’s important to remember about these guys?

Answer 22

1. gastrointestinal symptoms such as diarrhea and other
   - More severe possible symptoms include weight loss, anemia, lethargy and vomiting
   - May cause “Pseudo-Addison’s
2. Trichuris eggs are very resistant and may persist up to years in the environment

Question 23

Topic: Dipylidium spp.; Dipylidium caninum
1. What is the domestic small animal DEFINITIVE host? C/S
2. Where are the worms located?
3. List the routes of transmission.
4. How is it diagnosed?
5. How is it treated? **
6. How is it prevented?

Answer 23

1. dog, cat; In some cases, no clinical signs are noted; Some pets may “scoot” due to perianal irritation; Some cases may have non-specific gastrointestinal symptoms
2. Location: small intestine
3. Ingestion of infected intermediate host (most commonly
   fleas or lice). Gravid proglottids are voided in pet’s feces
4. Visualization of proglottid segments in feces
   and/or around perineal area or in the environment. Confirmation can be achieved by breaking open
   proglottids, adding saline and looking under
   microscope to identify packets and/or individual eggs.
   - Identification of egg packets on fecal floatation is rare
5. Praziquantel, Epsiprantel
6. Prevent ingestion of intermediate host. In addition to treating pet for D. caninum, make sure pet is receiving adequate flea and lice control

Question 24

Topic: Taeniid spp.
1. What is the domestic small animal DEFINITIVE host? C/S
2. Where are the worms located?
3. List the routes of transmission.
4. How is it diagnosed? ***
5. How is it treated?
6. How is it prevented?

Answer 24

1. Dogs: T. pisiformis (most common)
2. In some cases, no clinical signs are noted. Some pets may “scoot” due to perianal irritation. Some cases may have gastrointestinal impaction
3. Taenia pisiformis: ingestion of intermediate host (rabbit) tissue that contain cysticerci
4. • Identification of proglottids on fecal material
   • Fecal float (high specific gravity) to look for eggs
   • Not always seen on fecal float because proglottids are not distributed evenly through fecal material
   • Additionally, eggs do not float consistently
   • Note: Taenia eggs are indistinguishable from Echinococcus eggs under the microscope
5. Praziquantel, Epsiprantel, Fenbendazole
6. Elimination of predatory activities

Question 25

Topic: Echinococcus spp.

1. What is the domestic small animal DEFINITIVE host? C/S
2. Where are the worms located?
3. List the routes of transmission.
4. How is it diagnosed? ***
5. How is it treated?
6. How is it prevented?

Answer 25

1. dogs
2. SI
3. Gravid proglottids are shed in feces
   - Intermediate host (usually rodents) ingests the eggs and hydatid cysts develop
   - Definitive host becomes infected by ingesting intermediate host containing multilocular cysts
4. Difficult to identify visually due to small size
   b. Requires testing such as CELISA or PCR to diagnose
   c. Note: Echinococcus eggs are not distinguishable from Taenia eggs under the microscope
5. Praziquantel

Question 26

Topic: Canine Hip Dysplasia
1. What is this disease characterized by?
2. What breeds are most at risk of developing hip dyplasia?
3. When are juvenile diagnoses made?
4. List the clinical signs seen in patients.
5. What diagnostics should you run? What is seen?
6. How is this disease treated?
7. How can this disease be prevented?

Answer 26

1. This disease is characterized by instability of one or bot hip joints, leading to degenerative joint disease, OA, and subluxation of the hip.
2. German Shepherd, Golden Retriever, Labrador Retriever
3. 3-8 mo of age
4. • Pain on hip extension
   • Positive ortolani sign
   • Bunny hopping gait
   • Palpable crepitation over the hips
5. Ortho exam, xrays
   - Seen on xray:
   - Morgan line- osteophyte formation at insertion of joint capsule
   - Less than 80% coverage of femoral head
   - Remodeling, sclerosis & thickening of femoral neck
   - Joint laxity (see Penn HIP)
   - Perichondral osteophyte formation
   - Remodeling and sclerosis of the acetabulum
6. Over 80% of dogs will improve with conservative management but c/s will return later in life due to progression of degenerative changes.
   –> Conservative Management:
   - NSAIDs, weight management, nutraceuticals, conservative exercise

–> Surgical:
- Juvenile pelvic symphysiodesis: A procedure in which you cauterize or staple the growth plate in a dog 14-20 weeks of age. This encourages more acetabular coverage of the femoral head as the dogs grows. No improvement of hip dysplasia if it was severe pre-op; DJD still progresses.
- TPO
- Total Hip

7. Prevent over-nutrition; Over-nutrition during growth is related to a higher incidence of hip dysplasia. Conscious breeding

Question 27

A triple pelvic osteotomy involves three cuts: the _______, ______, and ______ and placement of a special plate on the ______ to ______ the pelvis. This should result in ________ acetabular coverage of the femoral
_________ as the patient matures. Want to perform at ___ mo - ___ mo of age. Patient is not a good candidate if there is any
evidence of _____ or subjectively the surgeon feels there is too much ______.

Answer 27

A triple pelvic osteotomy 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. Want to perform at 6 mo - 12 mo of age. Patient is not a good candidate if there is any
evidence of DJD or subjectively the surgeon feels there is too much laxity

Question 28

Topic: Cranial Cruciate Ligament Rupture

1. Where does the cranial cruciate ligament originate? Where does it insert?
2. What is the function of the CCL?
3. Is there a breed predisposition? Is there a specific age range?
4. What are the clinical signs?
5. What diagnostics should you run?
6. Treatment?

Answer 28

1. It originates on the medial surface of the lateral femoral condyle and inserts onto the craniomedial surface of the tibial plateau beneath the intermeniscal ligament.
2. Prevent cranial drawer, excessive hyperextension and internal rotation.
3. German Shepherds, Golden Retrievers, Labs, Boxers, Newfoundlands, Mastiff, Akita, etc.
4. Acute or chronic lameness that does not improve with rest, sit with knee rotated outward (positive sit test) +/- mild improvement with NSAID therapy.
5. Ortho exam, xrays
   - Positive cranial drawer, Positive tibial compression test (tibial thrust), Painful on extension.
   - Osteophytes typically present, especially along femoral trochlear ridge, tibial plateau, and patella; Joint effusion
6. Lateral suture, TPLO, TTA, cage rest for small dogs/owners who can not afford surgery; TPLO is gold standard.

Question 29

How do you perform a cranial drawer test?

Answer 29

One hand is placed on the distal femur with the thumb behind the lateral condyle. The other hand is placed on the proximal tibia with the thumb behind the fabella.

Question 30

Lateral Suture (______ Repair) Heavy suture placed around ________ on ______ aspect and then through a hole in the _____. This runs in similar orientation as the original cranial cruciate ligament except your prosthesis is _______ the joint (“________ repair”).
● Usually done on smaller dogs <___ kg .
● Can ? resulting instability

Answer 30

Lateral Suture (Extracapsular Repair)
● Heavy suture placed around fabella on lateral aspect and then through a hole in the tibia. This runs
in similar orientation as the original cranial cruciate ligament except your prosthesis is outside the
joint (“Extracapsular repair”).
● Usually done on smaller dogs <20kg .
● Can cycle, stretch, and break resulting instability

Question 31

Tibial Plateau Leveling Osteotomy
Osteotomy is performed at ________ _____ and the tibial ________ is then rotated and then stabilized
with a bone _____. This biomechanically changes the leg such that there is more load on the _______
cruciate ligament (which can handle the load) and you eliminate tibial _____.
● You did not fix the cranial cruciate ligament. Therefore, you will always have cranial _______.
However, the leg will be dynamically stable and prognosis is _______.

Answer 31

Tibial Plateau Leveling Osteotomy
● Osteotomy is performed at proximal tibia and the tibial plateau is then rotated and then stabilized
with a bone plate. This biomechanically changes the leg such that there is more load on the caudal
cruciate ligament (which can handle the load) and you eliminate tibial thrust.
● You did not fix the cranial cruciate ligament. Therefore, you will always have cranial drawer.
However, the leg will be dynamically stable and prognosis is excellent.

Question 32

Tibial Tuberosity Advancement
● Cut along ______ aspect of _____ tibia.
● Insert a _____ in between the tibia to advance it.
● Goal is to make ________ tendon ________ to the tibial plateau.
● This results in elimination of tibial thrust similar to the TPLO.
● Newer procedure, but early results are comparable to TPLO thus far.

Answer 32

Tibial Tuberosity Advancement
● Cut along cranial aspect of proximal tibia.
● Insert a cage in between the tibia to advance it.
● Goal is to make patellar tendon perpendicular to the tibial plateau.
● This results in elimination of tibial thrust similar to the TPLO.
● Newer procedure, but early results are comparable to TPLO thus far.

Question 33

Canine Elbow Dysplasia is an umbrella term for several congenital abnormalities that are recognized in the elbow. A dog with elbow dysplasia may be affected with

Answer 33

Ununited anconeal process (UAP), osteochondrosis
dissecans (OCD) of the humeral condyle, fragmentation of the medial coronoid
process (MCP), and elbow incongruity.

Question 34

Topic: Ununited Anconeal Process

1. What breeds are commonly affected?
2. What are the clinical signs seen?
3. What diagnostics do you run?
4. Tx?

Answer 34

1. German Shepherds!!!! Basset Hound, Bloodhound, Lab Retriever, Newfoundlands
2. By 4-12 months you will see forelimb lameness with pain on flexion and extension.
3. Physis should be closed by 4-5 months of age
   - Radiographs: visualize un-united anconeal process best on flexed lateral projection.
4. Can try medical management with NSAIDS but usually unrewarding. Excision of anconeal process seems to provide most consistent results

Question 35

Topic: OCD of Humeral Condyle

1. Definition
2. What are potential contributing factors?
3. Common breeds affected?
4. What are the clinical signs seen?
5. What diagnostics do you run?
6. Tx?

Answer 35

1. Abnormal endochondral ossification resulting in thickening of the articular cartilage
2. Growth rate, genetics, hormonal imbalance, and diet
3. German Shepherds, Golden Retrievers, Labrador Retrievers, Newfoundlands, Rottweiler
4. By 4-7 mo of age you will see forelimb lameness, pain on flexion and extension of the elbow joint; Bilateral disease at least 50% of the time
5. Xrays
   - See lesion on medial aspect of humeral trochlea
   - May see visible flattening
   - Subchondral bone defect & surrounding sclerosis
   - Osteophytosis
6. Surgical removal of flap and debridement of subchondral bone gives fair to excellent results with most dogs.
   - Typically performed arthroscopicall

Question 36

Topic: Medial Fragmented Coronoid Process
1. Common breeds affected?
2. Clinical signs?
3. Diagnostics
4. Tx

Answer 36

1. Labrador Retrievers, Golden Retrievers, Newfoundlands, Rottweilers
2. Usually by 4-7 months of age you will see Forelimb lameness and pain on flexion and extension of elbow
   ● May be bilateral
3. rads - Medial coronoid process may be large, blunted, or have osteophyte associated with it on the lateral view
4. Surgical removal of the fragment or arthroscopy for removal of fragment are most common treatments.

Question 37

Topic: Ethylene Glycol Toxicity

1. Ethylene glycol is found in?
2. How does it taste to animals?
3. Describe the pathophysiology of ethylene glycol toxicity.
4. Describe the c/s seen in each stage of EG toxicity.
5. How is this treated?
6. What is the prognosis?

Answer 37

1. Most commercial antifreeze
2. Sweet
3. Ethylene Glycol is metabolized into alcohol dehydrogenase –> glycoaldehyde –> glycolic acid –> glyoxalate and oxalic acid
4. • Stage 1: 30 min - 12 hrs post ingestion –> Neuro phase/ drunken behavior, anorexia, vomiting, PU/PD, Ca oxalate crystalluria
   • Stage 2: 12-24 hrs post ingestion –> Cardio phase where you see tachypnea and tachycardia, often unnoticed
   • Stage 3: 12 -72 hrs post ingestion –> Renal failure, MA, elevated osmolar gap, HypoCa, HyperGlucosemia
5. In order for tx to be effective, you must start tx before toxic metabolites are generated.
   - Fomepizole = inhibits alcohol dehydrogenase; most effective within 8 hrs of ingestion; very expensive
   - 20% ethanol = competitively inhibits alcohol dehydrogenase, less effective than Fomepizole but useful within 4-8 hrs of ingestion; Can worsen C/S
   - GI protectants, IVF, Diuretics
6. Prognosis is good if therapy started within 4-8 hrs. Guarded if patient is azotemic. Grave if oliguria/anuria present w/o dialysis treatments.

Question 38

Topic: Household Cleaner Toxicity

1. Ingestion of non-dilute acids and alkalis cause?
2. How is this treated? What should you not do and why?

Answer 38

1. Acids = burns in mouth, esophagus, and stomach; Alkali = lesions appear in 8-12 hrs
2. Dilute milk or water, GI protectants for several days, monitor for development of ulcers
   - DO NOT induce vomiting because this will further damage the esophagus.
   - DO NOT administer activated charcoal as that will bind acids and alkalis.

Question 39

Topic: Painting and Varnishing Products Toxicity

1. Most household paints and varnishes are?
2. What should be used to remove paint from fur?
3. What happens if paint thinners are ingested?

Answer 39

1. Nontoxic and only cause mild GI upset.
2. Do not use paint thinners or turpentine as that can be irritating and painful to skin and foot pads.
3. If ingested, administer dilute milk or water, GI protectants; DO NOT induce vomiting due to risk of aspiration pneumonia.

Question 40

Topic: Moldy Garbage Intoxication

1. What toxin is found in moldy food?
2. List the c/s
3. How is this disease diagnosed?
4. How is this treated?

Answer 40

1. Penitrem A, a neurotoxicant produced by Aspergillus spp.
2. Panting, restlessness, hypersalivation, Incoordination and fine motor tremors **, Can progress to tonic spasms, hyperthermia, ataxia and seizures
3. History, P vomiting up large amounts of garbage.
4. Induce emesis ONLY if not neurologically compromised/recumbent, Activated charcoal, methocarbamol for muscle tremors, diazepam or phenobarb for seizures, GI protectants.

Question 41

Topic: Anticoagulant Rodenticide Toxicity

1. List the different forms of anticoagulant rodenticide.
2. What is the toxic effect that this rodenticide has on the body?
3. What are the c/s seen?
4. What diagnostics should you run?
5. How is this treated?

Answer 41

1. Warfarn - 1st gen, brodifacoum and bromidialone - 2nd gen, Diphacinone (indandione).
2. The toxic effect is by inhibiting Vitamin K1 epoxide reducatase –> prevents activation of vit K dependent coag factors 2,7,9,10
3. Depends on location and severity of hemorrhage; commonly in body cavities, hemmorhagic shock - pale mm, prolonged CRT, tachycardia, weak pulses, abdominal distension, resp distress. These signs typically occur 3-7 days post ingestion but compounds and persists for 4-6 weeks.
4. • PT/PTT: prolonged for both. Takes 36-72 hrs for PT because that depends on Factor 7 which has the shortest half life of all vit k dependent coag factors. PTT takes 3-5 days to see.
5. • If within 2-4 hrs induce emesis.
   • If within 8-12 hrs give AC +/- sorbitol
   • Treat with Vit K1 for 4 weeks OR check PT 36-72 hrs later to determine if Vit K1 is needed.
   • Check PT 48-72 hrs after completion of Vit K1.

• If O is unsure if P ingested rat bait or not, only induce emesis if PT is normal. Perform PT, put on Vit K1, check Pt 48-72 hrs after completion of Vit K1.
• if P is presenting with hemorrhage secondary to coagulopathy, need ot give plasma transfusion ASAP because plasma is needed for immediate hemostasis.

Question 42

Topic: Bromethalin Rodenticide Toxicity
1. What is the toxic principle ?
2. Clinical signs?
3. Tx

Answer 42

1. Inhibits oxidative phosphorylation and ATP production, especially in neurons –> Loss of ability to maintain osmotic gradients, cerebral edema, increased intracranial pressure.
2. If ingested a high dose, will see tremors, seizures, hyperexcitability, and hyperthermia < 12 hrs post-ingestion. If ingested a lower dose, won’t see signs for a few weeks post ingestion then will see ascending paralysis beginning in the hindlimbs.
3. If acute, gastrointestinal decontamination (emesis or gastric lavage and activated charcoal)
   ● Once clinical signs present, largely symptomatic/supportive care
   a. Seizure treatment/prophylaxis
   b. Treatment for increased intracranial pressure
   i. Mannitol and/or furosemide to reduce cerebral edema
   ii. Incline plane 30° to promote venous return
   ● Severe clinical signs warrant poor prognosis

Question 43

Intervertebral Disc Disease: Thoracolumbar and
Cervical

Horner’s Syndrome

Cervical Vertebral

Instability (Wobbler Syndrome)

Patellar Luxation

Osteoarthritis (Degenerative Joint Disease)

Question 44

Topic: Cholecalciferol Rodenticide Toxicity

1.What is the toxic principle ?
2. Clinical signs? Diagnostics
3. Tx

Answer 44

1. Precursor converted into active Vitamin D after ingestion –> increased intestinal absorption of calcium and mobilization from bones –> severe hypercalcemia, hyperphosphatemia and organ injury.
2. PU/PD, GI upset, Acute renal failure, cardiac arrhythmias.
   - Presence of hyperphosphatemia (12 hrs post-ingestion), hypercalcemia (24 hrs post) and
   azotemia (36-48 post).
3. If acute, emesis and activated charcoal

• Hypercalcemia present
  a. Saline diuresis and loop diuretic (i.e. furosemide) to promote urinary calcium excretion.
  b. Corticosteroids can be used to decrease intestinal Ca absorption and urinary retention.
  c. Bisphosphonates (pamidronate) inhibit osteoclast activity and bone re-absorption.
• Azotemia present
  a. Supportive care for acute renal failure.
  b. Prognosis guarded to grave once progression to renal failure occurs.

Question 45

Topic: Canine Soft Tissue Sarcomas

Soft tissue sarcomas (STS) in dogs are composed of a variety of tumors derived from ________ cell origin. These tumors include ?
These tumors are all grouped together because they all
share the same biologic behavior. They are all _______ invasive while their
potential for metastasis can be determined by their ?

Answer 45

Soft tissue sarcomas (STS) in dogs are composed of a variety of tumors derived
from mesenchymal cell origin. These tumors include peripheral nerve sheath tumors
(PNST), hemangiopericytomas (HPC), fibrosarcomas (FSA), liposarcomas, malignant
fibrous histiocytomas, myxosarcomas, rhabdomyosarcomas, leiomyosarcomas, etc.
These tumors are all grouped together because they all
share the same biologic behavior. They are all locally invasive while their
potential for metastasis can be determined by their histologic grade.

Question 46

Topic: Canine Soft Tissue Sarcomas

Constitute ____% of all skin and SQ tumors in dogs
● All are very _____ invasive regardless of grade
● Treatment is aimed at ________ removal with ______ margins
● _______ recurrence is common following conservative excision.

Answer 46

Constitute 15% of all skin and subcutaneous tumors in dogs
● Common histologies affecting the skin and subcutaneous tissue include FSA, PNST, and HPC
● All are very locally invasive regardless of grade
● Metastatic potential can be determined by histologic grade
● Treatment is aimed at surgical removal with wide margins
● Local recurrence is common following conservative excision.

Question 47

Topic: Canine Soft Tissue Sarcomas

1. How do you diagnose these tumors?
2. How do you tx these tumors?

Answer 47

1.
- FNA: May be read out as “spindle cell proliferation” in well-differentiated tumors
● Most exfoliate poorly leading to sparsely cellular samples
- Biopsy: Occasionally required for diagnosis if FNA is non-diagnostic
● Required for grading
- Thoracic rads to check for metastasis
- CT or MRI recommended for surgical planning
2. Wide excision with a minimum of 3 cm margins is ideal in locations that are amenable
to such a surgery. Amputation not recommended.
- Radiation therapy recommended if surgical margins are incomplete or narrow.
- Consider chemo if metastasis is present, high grade tumor, or at visceral site. (Adriamycin (doxorubicin) based chemo protocols are most commonly used.)

Question 48

Topic: Canine Soft Tissue Sarcomas

1. What is the prognosis?
2. What are the control rates?

Answer 48

Grading
● Biopsy required for grading
● Gives probability of metastasis
a. Low or intermediate grade tumors have a < 20% chance of metastasis.
b. High grade tumors have a 40-50% chance of metastasis.
● Factors assessed for grading
a. Differentiation of tumor
i. Well differentiated, moderately differentiated, or poorly differentiated.
b. Percent necrosis in tumor
i. No necrosis, <50% necrosis, >50% necrosis.
c. Mitotic index
i. <10 mitoses/10 high power fields, 10-19 mitoses/10 high power fields,
>19 mitoses/10 high power fields.
Control Rates
● Incomplete surgical excision with adjuvant radiation therapy.
a. 95% 1 year control
b. 85% 3 year control
c. 75% 5 year control
● Only up to 1/3 of affected dogs die of tumor related causes.

Question 49

Topic: HSA

Hemangiosarcoma (HSA) is a malignancy of ________ cells that normally line _______ _______. It can develop any place in the body that has _______ ______, but
most commonly occurs in the ______ of dogs. Another form of the disease is the
________ form, which is induced by ?

Answer 49

Hemangiosarcoma (HSA) is a malignancy of endothelial cells that normally line
blood vessels. It can develop any place in the body that has blood vessels, but
most commonly occurs in the spleen of dogs. Another form of the disease is the
cutaneous form, which is induced by ultraviolet radiation from the sun. Because
of the biological differences between the cutaneous and visceral forms of the
disease, we will discuss each of them separately in this PowerPage.

Question 50

Topic: Hemangiosarcoma

Most commonly affects ______ breed dogs such as ?
a. Most commonly affected organ is the _______
i. Other commonly affected organs include the ?
● The most common tumor to metastasize to the _____
● Often present through emergency for acute ______ and _______ shock, or pericardial _____ and _______ shock.
a. May have history of “good days” and “bad days” associated with small bouts of internal
_________ and re-absorption of the blood.
● Highly metastatic via blood vessels and direct contact seeding within the abdomen
if tumor ruptures.
● Median survival times generally do not exceed ___ ______, regardless of treatment.

Answer 50

Most commonly affects large breed dogs such as German Shepherd Dogs, Golden Retrievers,
Labrador Retrievers, etc.
a. Most commonly affected organ is the spleen
i. Other commonly affected organs include the right atrium (auricle), liver,
retroperitoneal space, subcutaneous tissue.
● The most common tumor to metastasize to the brain
● Often present through emergency for acute hemoabdomen and hypovolemic shock, or pericardial.
effusion and cardiogenic shock.
a. May have history of “good days” and “bad days” associated with small bouts of internal
hemorrhaging and re-absorption of the blood.
● Highly metastatic via blood vessels and direct contact seeding within the abdomen
if tumor ruptures.
● Median survival times generally do not exceed 1 year, regardless of treatment.

Question 51

Topic: HSSA

1. How do you diagnose HSA? What do you see?
2. Tx?
3. Prognosis

Answer 51

1. • AUS: HSA often appears cavitary and fluid-filled; Also used to identify free abdominal fluid, primary and metastatic lesions, especially in the liver, lymph
     nodes, and serosal surfaces.
   • FNA + cytology: unrewarding
   • Surgical biopsy: Splenectomy recommended for suspected splenic lesions or for those with a chance of rupturing (cavitary, large, fluid-filled). Incisional biopsies (Tru-cut, punch biopsy, etc.) that do not remove the entire tumor run the risk of hemorrhage.
   • Thoracic radiographs: To identify pulmonary metastasis and pericardial effusion.
   • **CBC, chemistry panel, urinalysis: Common findings: anemia (with or without regenerative response), thrombocytopenia, presence of schistocytes
   • Cardiac ultrasound
   • Coagulation panel
   • CT or MRI
2. Resuscitate and stabilize with IV fluids and blood products as necessary for hemoabdomen.
   ● Exploratory surgery to remove the primary tumor and biopsy abnormal tissues.
   ● Adriamycin-based chemotherapy to help delay development of metastasis and prolonged survival
3. Prognosis of the splenic form depends on the stage of the disease and whether or not Adriamycin
   is administered:
   ● Surgery alone: median survival time 3 weeks-3 months
   ● Stage I – single lesion without hemorrhage and treated with surgery and Adriamycin-based
   chemotherapy: 9 months.
   ● Stage II – single lesion with hemorrhage and treated with surgery and Adriamycin- based
   chemotherapy: 5-6 months .
   ● Stage III – metastasis present treated with Adriamycin chemotherapy: 3.5 months

Question 52

Topic: Cutaneous Hemangiosarcoma

1.

Answer 52

Induced by chronic sun exposure
● Dogs with increased risk:
a. Breeds with unpigmented skin and white haircoat, thin short hair, high amounts
of sun exposure.
b. Fawn colored Pit Bulls, Whippets, Dalmations, English Pointers, etc.
● Commonly affected sites:
a. Sparsely haired areas
b. Ventral abdomen and medial thighs
c. All sun-exposed areas are abnormal and have potential to undergo malignant transformation
and form multiple tumors.
d. Can occur in conjunction with solar-induced squamous cell carcinoma.
● Biological behavior is different from visceral and subcutaneous forms of HSA
a. About 1/3 may metastasize and are more likely associated with advanced, invasive forms
of the disease.
Treatment
● Surgery to remove invasive or problematic (bleeding, infected) lesions.
● Prevention: apply sunblock or keep indoors during intense sunlight hours for dogs with thin hair
coats and unpigmented skin.
Prognosis
● May live for years with these tumors.
● New tumors will form since all of the affected skin is abnormal.

Question 53

Topic: Canine Oral Melanoma

1. This is considered to be the?
2. Most commonly seen in what breeds?
3. This is a tumor of?
4. About 1/3 of these tumors are?
5. How is diagnosing them challenging?
6. Most OMM cases are?
7. Most commonly found where in the body?

Answer 53

1. most common malignant oral tumor in the dog
2. Chow Chows, Golden Retrievers, Poodles, and Cocker Spaniels.
3. Melanocytes
4. Amelanotic and may not contain any melanin
5. Morphologically, OMM can look like neoplasms of mesenchymal (sarcoma), epithelial (carcinoma), or round cell origin.
6. <etastatic (up to 80%) ; frequently metastasize to local lymph nodes and then the lungs.
7. Besides the oral cavity, Cutaneous (more commonly benign), in nail beds (about 50% are malignant and 50% are benign).

Question 54

Topic: Canine Oral Melanoma

1. How do you definitively diagnose ?
2. What should staging include?
3. What diagnostics are often helpful?
4. How is this treated?
5. Prognosis

Answer 54

1. Biopsy is needed to definitively diagnose OMM
2. Minimum database, Regional lymph node aspirates, Thoracic radiographs
3. Cross sectional imaging with CT or MRI are often helpful in assessing bone involvement and in
   surgical planning
4. Treatment of choice for the primary tumor is surgical excision with wide margins, which usually
   necessitates removal of underlying bone (partial mandibulectomy or maxillectomy).
   - Radiation therapy is useful in shrinking the tumor or temporarily slowing its growth if surgical
   excision is not an option or if there is high chance of local recurrence; carboplatin and cisplatin, have shown mild efficacy in temporarily shrinking gross OMM lesions.
5. • Tumors size: tumors <2cm have a median survival time of about 17 months
   • > 2cm have a median survival of about 5.5 months
   • Tumor location: dogs with tumors in the rostral oral cavity have longer median survival rates
     than those in the caudal oral cavity

Question 55

Topic: OSA

1. This is considered to be the most?
2. Most common in what breeds? In what parts of the body?
3. How is this disease diagnosed? What is seen in each?
4. Treatment?

Answer 55

1. Common primary bone tumor in dogs
2. Most commonly occurs in large and giant breed dogs in the metaphyseal regions of the
   appendicular skeleton. Distal radius, proximal humerus, distal femur, proximal tibia (“away from the elbows and toward the knees”).
3. • limb rads: Classically a lytic and productive lesion at the metaphysis of the bone. Do not cross joints into adjacent bones.
   • FNA + cytology: Aspirate the center of the lesion often result in “reactive bone”; possibility of pathologic fracture with aspiration or biopsy.
   • Biopsy: May be required for a definitive diagnosis in equivocal cases.
   • Thoracic rads: Pulmonary metastasis visible in less than 10% of cases at the time of diagnosis but will develop in the future in most cases.
   • bone scan or nuclear scintigraphy: Used to find or rule out suspected bone metastasis.
   • Bloodwork: Elevation in alkaline phosphatase on a chemistry panel is associated with a worse prognosis.
4. Amputation is the most effective way to alleviate pain of bone destruction. Palliative as most dogs will develop metastasis in the future
   - Limb sparing procedures have a high rate of chronic resistant infections, tumor recurrence, etc.
   - radiation?
   - chemo?

Question 56

How do bone scans or nuclear scintigraphy work?

Answer 56

Technetium-99–hydroxymethylene diphosphonate binds to areas of active bone and is detected in imaging.
● Sensitive, but poorly specific.
a. Increased uptake can occur with bone tumors, arthritis, fractures, or osteomyelitis.
● Alternatively, full body radiographs can be performed.

Question 57

Radiation and chemo - OSA

Answer 57

radiation:
Can be effective in palliating the pain of bone tumors in up to 75% of cases, for about 2- 3 months.
a. No detectable improvement in pain in 25%.
● Pathologic fractures may be more likely to occur if pain is well controlled and use of
the limb is increased.

chemo Proven to extend survivals over surgery alone.
● Chemotherapy protocols mostly consist of a platinum drug (cisplatin or carboplatin) as a single
agent or in conjunction with Adriamycin (doxorubicin).
● Generally thought not to be effective if macroscopic disease is present.
● Bisphosphonates (pamidronate) are osteoclast inhibitors that can help palliate pain in patients
where surgery is not an optio

Question 58

osa:
Median Survival Times
● Amputation alone: 4-6 months.
● Surgery (amputation or limb spare) with chemotherapy: 10-12 months.
● Presence of macroscopic metastatic disease: 1-3 months

Question 59

Axial Osteosarcoma
● Make up ǻǾ% of all OSAs and occur more commonly in small- or medium-sized dogs compared to
appendicular OSA.
● Common locations: mandible, maxilla, scapula, ribs, spine, pelvis.
● The mandible has a better prognosis compared to all other sites.
a. Ȁǹ% Ǻ-year survival with surgery alone.
● Other locations generally thought to have aggressive clinical courses similar to the
appendicular disease

Question 60

Topic: KCS

Question 61

Topic: Glaucoma
1. List the major clinical signs
2. How do you diagnose glaucoma?
3. How is this tx?
4. Prognosis?

Answer 61

1. Bupthalmos; big blue eye, Visual impairment, tortuous episcleral vessels
2. Tonometry: IOP > 30 mmHg, Ocular US, gonioscopy to look at iridocorneal angle
3. Topical or systemis: carbonic anhydrase inhibitor, beta-adrenergic antagonist, IV mannitol, +/- topical or systemic corticosteroids
   - CAI = dorzolamide
   - Prostaglandin analogue = Latanoprost
4. Always treat contralateral eye prophylactically. Treat even if blind to address pain.

Question 62

Topic: SARDS

Question 63

Topic: Corneal Ulcers

Question 64

Topic: Cataracts

1. List the major clinical signs
2. How do you diagnose glaucoma?
3. How is this tx?
4. Prognosis?

Answer 64

1. Cloudy white pupil, decreased vision.
2. Blood and urine glucose, ocular US, electroretinography
3. Surgery
4. Good to excellent with surgery

Question 65

Topic: Uveitis
1. List the major clinical signs
2. How do you diagnose glaucoma?
3. How is this tx?

Answer 65

1. Conjunctival hyperemia, photophobia, blepharospasm, aqueous flare (cloudiness of aqueous humor), color change of iris, midrange to miotic pupils.
2. Tonometry: IOP < 10 mmHg, BW to look for underlying cause
3. Topical or systemic corticosteroids or NSAIDs unless secondary to protozoal or fungal infection or corneal ulceration, topical atropine for pain, treat underlying cause

Question 66

Topic: Fleas & Flea Allergy Dermatitis

1. This is the most common cause of?
2. What is the most common flea for both dogs and cats?
   2a. What potential pathogens does this flea carry?
   2b. How many eggs does this flea lay per day? It lays eggs within what amt of time?
   2c. What is the average time it takes for the flea to complete its life cycle?
   2d. What dermatologic conditions does this flea cause?

Answer 66

1. Pruritus in dogs and cats
2. Ctenocephalides felis felis
   2a. Bartonella henselae, Dipylidium caninum, and Yersinia Pestis
   2b. 27 eggs/day; lays eggs every 24-36 hrs
   2c. 3 weeks ; in perfect conditions - 16 days.
   2d. Flea infestation: leads to mild to moderate pruritus; Flea allergy dermatitis: patient is actually allergic to the flea saliva. This is a Type 1, 4, and basophil hypersensitivity. The salivary enzymes contain proteolytic enzymes, histamine-like compounds, anti-coagulants, haptens and antigens

Question 67

Topic: Fleas & Flea Allergy Dermatitis cont.

1. What are the clinical signs associated with flea infestation and flea allergy dermatitis?
2. Describe the distribution of the side effects of these conditions?
3. Flea infestation is a common cause of what other disease in cats?
4. How do you diagnose flea infestation and flea allergy dermatitis in dogs and cats?
5. How is this disease treated?

Answer 67

1. Intense pruritus, erythema, alopecia, papules, pustules, excoriations, crusts, and moist dermatitis. Hyperpigmentation and lichenification may develop in more chronic lesions.
2. In dogs - Caudal-dorsal distribution aka Base of tail, posterior/lateral aspect of rear legs and ventral abdomen; In cats - Often neck and face
3. Common cause of miliary dermatitis and
   eosinophilic granuloma complex
4. C/S, flea dirt, intradermal testing
5. A. Symptomatic and palliative therapy - Short term glucocorticoids
   B. Environmental flea Control - treat each animal in house, deep clean environment; will take 2-3 mo for fleas to be properly eliminated b/c pupa stage is 1-2 mo and is very resistant to environmental treatments.
   C. Adulticides
   D. Insect growth regulators

Question 68

How do flea adulticides work?

Answer 68

Eliminates fleas present on animal but does not prevent re-infestation. Depending on the product, may take minutes to 48 hours.

Ex: Fipronil (toxic to rabits), Fluralaner, Alfoxalaner, etc.

Question 69

How do insect growth regulators work? Give examples.

Answer 69

Disrupt developmental process.
Ex: Lufenuron, Pyriproxifen, S-methoprene

Question 70

What flea repellent repels via physical contact?

Answer 70

Permethrin; toxic to cats

Question 71

What is the etiology of Zinc Responsive Dermatosis in dogs?

Answer 71

The exact cause is unknown, but it is proposed to be due to a defect in intestinal absorption of zinc. Tx with zinc supplementation. Response to tx is seen within days.

Question 72

Topic: Discoid Lupus Erythematosus (DLE) in dogs

1. What are the c/s?

Answer 72

1. Clinical signs consistent with DLE include depigmentation of the nasal planum, erythema, scaling, and loss of the “cobblestone” appearance of the nasal planum. Alopecia, crusting, scaling, and ulcerations can also be seen on the face, muzzle, lips, pinnae, and periorbitally.

Question 73

Localized, juvenile-onset demodicosis usually resolves without treatment as the immune system develops. Because this patient only has a small area of alopecia and few mites, starting therapy with ivermectin and Amitraz dips is pre-mature. Both these therapies have marked side effects. Ivermectin causes neurological signs, and Amitraz can cause allergic reactions, hypothermia, bradycardia, and hyperglycemia (especially in small puppies). Lime sulfur dips are not effective against follicular
Demodex mites (as found in dogs). Demodex gatoi is found in cats and is a superficial mite that can be treated with lime sulfur.

Question 74

What type of medication is Firocoxib?

Answer 74

An NSAID; do not give with steroid

Question 75

The correct answer is feeding a diet with novel protein and carbohydrate sources or a hydrolyzed diet.
Hydrolyzed diets are a good alternative to novel protein diets when the diet history is unknown or the pet has been exposed to many proteins. Hydrolyzed diets reduce the size of the protein and thus minimize the ability to cross link with IgE and cause mast cell degranulation. Antihistamines, corticosteroids, and hyposensitization treatments are used for atopic patients. If food allergy is the animal’s only problem, it should resolve with feeding a diet with novel protein and carbohydrate sources.

Question 76

Topic: Sarcoptes

A superficial skin scrape is most useful. A deep skin scrape is used for Demodex mites, which reside in the hair follicles. Superficial skin scraping is indicated for Sarcoptic mange, since this mite lives in the stratum corneum. Pinnal-pedal reflex can be positive in 70% of Sarcoptic mange infestation but can also be positive in any dog with pruritus. Clinical signs are helpful because Sarcoptes typically infects the non-haired portions of the skin such as the ear pinnae, elbows, hocks, and ventral abdomen. If the mite is not found on skin scraping and you have clinical signs indicative of Sarcoptes then a therapeutic trial is warranted. Keep in mind that in most cases you will not be able to find the mite.
A trichogram would not be indicated. This method can be used to diagnose dermatophytosis and sometimes Demodex. Histopathology will reveal a perivascular dermatitis that is non-specific. Rarely are the mites found on histopatholoov.

Question 77

Topic: Canine Familial Dermatomyositis

1. What breeds are predisposed?
2. What does the disease cause?
3. How is this treated?

Answer 77

1. Collies and Shetland Sheepdogs
2. Atrophy of muscles and erosion, crusting, and alopecia of skin which is exacerbated by heat and sun exposure.
3. This condition is treated with corticosteroids, Vitamin E, and omega-3 fatty acids. Often unrewarding