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 (aka immune destruction of the thyroid gland).
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), Hypercholesterolemia
   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 - PDC = both adrenals are plump; ADC = one is enlarged, the other atrophied/nonvisible.
   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? How is it transmitted?
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!!!
   - NOTE: Enrofloxacin has been associated with articular cartilage damage in rapidly growing dogs 2–8 months old and should be discontinued if joint pain or swelling develops.
   - 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

Topic: Pyometra

1. Define this condition.
2. Most common signalment
3. When does it typically occur? Explain why
4. List the clinical signs
5. How is this condition diagnosed?
6. How is this condition treated?

Answer 9

1. Pyometra is a bacterial infection of the uterus due to hormonal changes in unspayed dogs.
2. It is reported primarily in dogs more than 5 years old.
3. This condition tends to occur 4 to 6 weeks after estrus. After estrus, the level of progesterone stays high to prepare the uterus for pregnancy by thickening its surface. If pregnancy does not occur for several cycles, the lining inside the uterus continues to thicken and cysts can form within the uterus. These cysts and accumulated uterine fluids provide an ideal environment for bacterial infection. Pyometra can occur due to administration of estrogen- or progesterone-based medications.
4. The signs are variable and include lethargy, poor appetite, increased thirst and urination, and vomiting. When the cervix is open, a discharge of pus, often containing blood, is present. When the cervix is closed there is no discharge and the large uterus may cause abdominal enlargement. Signs can progress rapidly to shock and death.
5. The infection is diagnosed by physical examination, determination of the nature of the discharge, ultrasonography, x-rays, and laboratory and blood tests.
6. Removal of the ovaries and uterus (“spaying”) is the recommended treatment in most cases. For younger animals that are not seriously ill and that will be bred in the future, antibiotics, intravenous fluids, and prostaglandin can be administered. However, medical treatments carry higher risk in dogs with a closed cervix because the infected uterus may burst. Animals should be re-examined 2 weeks after completion of medical treatment to ensure complete emptying of the discharge from the uterus. Dogs with a history of pyometra should be bred on every heat cycle after treatment, as pyometra will eventually recur. Affected dogs should be spayed as soon as their breeding life is over.

Question 10

Topic: Congestive Heart Failure

1. List the classic clinical signs seen in patients with CHF.
2. What diagnostics would you run on a patient with possible CHF?
3. How is CHF treated?
4. What is the prognosis?

Answer 10

1. Dypsnea, tachypnea, exercise intolerance, cough
   - +/- abdominal distension, harsh lung sounds and crackles, heart murmur and arrhythmia
2. A. Radiographs:
   - In cases of left sided heart failure: pulmonary edema
   - In cases of right sided heart failure: ascites
   - Cardiomegaly
   - Dilated pulmonary veins
   - Interstitial to alveolar lung changes in caudo-dorsal lung fields
   B. Echocardiography:
   - Valvular insufficiency
   - Poor contractility
3. A. Acute CHF:
   - Oxygen supplementation
   - Furosemide (loop diuretic)
   - Pimobendan (positive ionotrope and vasodilator) OR nitrates (nitroglycerin - venodilator or nitroprusside - venodilator and arteriodilator)
   B. Chronic CHF:
   - Furosemide (loop diuretic)
   - Pimobendan (positive ionotrope and vasodilator)
   - Enalapril (ACE Inhibitor - acts on the enzyme ACE from converting angiotensin I into angiotensin II which narrows blood vessels –> increased blood pressure)
   - Restrict exercise
   - Low sodium diet
4. Prognosis is guarded :(

Question 11

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

Answer 11

1. DCM is a primary myocardial disease characterized by left-sided cardiac enlargement and impaired systolic function.
2. Doberman, Irish Wolfhound, Great Dane, St. Bernard, Newfoundland, Leonberger, Boxer, Giant Schnauzer, Cocker Spaniel, Flat Coat Retriever.
   - Genetic testing is available for Doberman Pinschers:
   - Pyruvate dehydrogenase kinase-4 (PDK4): NCSU DCM1 (10x more likely), NCSU DCM2 (20x more likely)
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 (d/t pulmonary edema) from left-sided congestive heart failure.
   - Abdominal distention from ascites from right-sided congestive heart failure
4. A. Echocardiogram (gold standard):
   - Systolic cardiac dysfunction (poor contractility and shortening fraction)
   - Dilated left atrium and ventricle
   B. ECGs: can see PVCs, v-tach, afib
   C. Radiographs
5. A. Subclinical dogs: ACE inhibitors and/or pimobendan for dogs with early stage cardiac dilatation.
   B. For dogs with arrhythmias: ventricular tachycardia (especially in Boxers and Dobermans), options include:
   - Sotalol (beta blocker)
   - Amiodarone (anti-arrhythmic)
   - Mexilitine (sodium channel blocker)
   - Very low dose Atenolol (beta blocker)

Question 12

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 12

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 13

Topic: Mitral Valve Dysplasia

Question 14

Topic: Toxocara spp.

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

Answer 14

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 15

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 15

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 16

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 16

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 17

Toxocara is also known as the canine/feline?

Where are the worms typically found?

What is important to note about Toxocara lenonina compared to canis and cati?

Do toxocara spp. possess zoonotic potential?

Answer 17

Roundworm

The small intestine

Migration does not occur outside of the GI tract compared to other Toxocara spp. !

Yes! Toxocara canis is implicated in visceral larval migrans in humans

Question 18

What parasite is this?

Answer 18

Toxocara canis from canine.

Question 19

What parasite is this?

Answer 19

Toxocara cati

Question 20

What parasite is this?

Answer 20

Toxocara spp. eggs

Looks like a little bowl with some miso soup in it!

Question 21

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

Answer 21

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 22

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 22

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 23

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 23

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 24

Ancyclostoma spp. is also known as ?

What is important to remember about Ancyclostoma spp. ?

Where are these worms mainly located?

Answer 24

The canine and feline hookworm

Ancylostoma spp are associated with high zoonotic potential. Associated with cutaneous larval migrans in humans

The small intestine

Question 25

What parasite is pictured here?

Answer 25

Ancyclostoma canis

Question 26

What parasite is pictured here?

Answer 26

Ancylostoma braziliense adult female

Question 27

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 27

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 28

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 28

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 29

What is an alternative name for Trichuris spp.?

What is important to remember about Trichuris spp.?

Where are these worms mainly located?

Answer 29

Whipworm

• May cause “Pseudo-Addison’s
• Due to intermittent shedding, density and small number of eggs, may be difficult to diagnose on fecal float
• Trichuris eggs are very resistant and may persist up to years in the environment

In the cecum!

Question 30

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 30

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 31

Dipylidium spp. are also called?

Where are these worms typically found?

Answer 31

Tapeworms

The small intestine

Question 32

What is this parasite called?

Answer 32

Dipylidium caninum

Question 33

What is the parasite pictured here?

Answer 33

Dipylidium caninum

Question 34

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 34

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 35

What parasite is pictured here?

Answer 35

Taeniid spp.

Looks like an upside down mushroom cap !

Question 36

What is important to remember about Taeniid spp.?

Answer 36

Taenia eggs are indistinguishable from Echinococcus eggs under the microscope

Question 37

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 37

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 38

What is important to remember about Echinococcus spp?

Answer 38

The internmediate host is usually a rodent?

Question 39

What parasite is pictured?

Answer 39

Echinococcus granulosus egg

Question 40

What parasite is pictured below?

Answer 40

Hyatid cyst of E. granulosus.

Question 41

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 41

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 42

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 42

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 43

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 43

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 44

How do you perform a cranial drawer test?

Answer 44

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 45

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 45

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 46

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 46

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 47

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 47

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 48

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 48

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

Question 49

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 49

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 50

Topic: Osteochondrosis Dissecans

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

Answer 50

1. Abnormal endochondral ossification resulting in thickening of the articular cartilage
2. Failure of immature cartilage to form bone in the (humeral head, elbow joint, etc) –> abnormal cartilage thickening –> malnourished cartilage cells die –> formation of a defect at the junction between cartilage and bone –> normal daily activity may cause fissures in the cartilage that eventually communicate with the joint, forming a cartilage flap.
3. Growth rate, genetics, hormonal imbalance, and diet
4. German Shepherds, Golden Retrievers, Labrador Retrievers, Newfoundlands, Rottweiler
5. 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
6. Xrays
   - Shoulder: Defect (flattening) present in the humeral head on X-rays of the shoulder. Older dogs that have chronically untreated OCD present with large calcified fragments “joint mice” and osteoarthritis.
   - Subchondral bone defect & surrounding sclerosis
   - Deposition of new bone
   - Ununited anconeal process, fragmented coronoid process
7. Surgical removal of flap and debridement of subchondral bone gives fair to excellent results with most dogs.
   - Typically performed arthroscopically

https://www.acvs.org/small-animal/canine-elbow-dysplasia/

https://www.google.com/search?sca_esv=3ec8625b255dccb3&q=fragmented+coronoid+process+dog+radiograph&udm=2&fbs=ABzOT_CWdhQLP1FcmU5B0fn3xuWpA-dk4wpBWOGsoR7DG5zJBr1qLlHFB6ZBcx-Arq68_wdJlnBwAHirUEMwdE4O8L3EsOBFudme3Tao3KPzT2BTFLr2mwwWDogIjAMMisnTxQF3jo-eMbkcqf6NRauwjSOZkIzuDxRHRvQjDldojY7n11qrNAseRBnsUiJfrjTwE9iBSeZON5KKLu12rw-UtNuhjMkMVw&sa=X&ved=2ahUKEwiR8u_a7PWLAxWIjYkEHVjvORsQtKgLegQIEhAB&biw=1406&bih=857&dpr=2

https://vetrica.com/osteochondrosis-in-the-dog/

https://www.ethosvet.com/blog-post/elbow-dysplasia-in-dogs/

Question 51

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

Answer 51

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 52

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 52

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 53

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 53

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 54

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 54

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 55

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 55

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 56

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 56

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 57

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

Answer 57

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 58

Topic: Cholecalciferol Rodenticide Toxicity

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

Answer 58

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 59

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 59

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 60

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 60

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 61

Topic: Canine Soft Tissue Sarcomas

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

Answer 61

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 62

Topic: Canine Soft Tissue Sarcomas

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

Answer 62

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 63

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 63

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 64

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 64

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 65

Topic: HSSA

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

Answer 65

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 66

Topic: Cutaneous Hemangiosarcoma

1.

Answer 66

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 67

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 67

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 68

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 68

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 69

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 69

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 70

How do bone scans or nuclear scintigraphy work?

Answer 70

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 71

Radiation and chemo - OSA

Answer 71

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 72

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 73

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 74

Topic: KCS
1. Describe the pathogenesis of this disease.
2. What is the etiology in dogs? Cats?
3. How is it diagnosed?
4. How is it treated?

Answer 74

1. Aqueous tear film deficiency. Usually bilateral and idiopathic that results in persistent conjunctivitis, mucopurulent discharge, superficial corneal vascularization, superficial corneal pigmentation, and fibrosis +/- corneal ulceration.
2. Occurs primarily in dogs, rarely in cats.
   Dogs: Most often associated with autoimmune dacryoadenitis (inflammation of the lacrimal gland) and destruction of both the lacrimal and nictitans glands.
   - Distemper, systemic sulfonamide, heredity, and trauma are less frequent causes of KCS in dogs.

Cats: Chronic feline herpesvirus 1 (FHV-1) infections that scar the conjunctiva and openings of the tear ducts.

3. A. Schirmer tear test = diagnostic test of choice
4. A. Artificial tear solutions and ointments: Cyclosporin, Tacrolimus, Pimecrolimus
   B. AM-corticosteroid cream IF NO CORNEAL ULCER

Question 75

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

Answer 75

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 76

Topic: SARDS

Question 77

Topic: Corneal Ulcers

Question 78

Topic: Cataracts

1. List the causes of cataracts in dogs.
2. Describe the pathogenesis.
3. List the major clinical signs
4. List the secondary complications of cataracts.
5. How do you diagnose glaucoma?
6. How is this tx?
7. Prognosis?
8. What could this condition be if the patient is NOT having difficulty seeing?

Answer 78

1. Genetic inheritance (Miniature Schnauzer), metabolic disturbances such as diabetes mellitus, trauma, nutritional imbalance such as orphaned puppies on milk replacer, and lastly chronic uveitis - an inflammatory disease of vascular tissue deep in the eye.
2. Protein accumulation –> Opaque lens –> light can not pass through retina –> blindness.
3. Cloudy white pupil, decreased vision, +/- painful (chronic cases).
4. Uveitis, glaucoma (increased intraocular pressures), and lens luxation (dislocation of the lens), +/- retinal detachment –> blindness.
5. Blood and urine glucose, ocular US, electroretinography
6. Surgery - phacoemulsification. Small incisions are made in the cornea and the lens capsule to pulverize the lens and remove it via vacuum. Surgery should not be performed if the cornea is unhealthy.
7. Good to excellent with surgery (80-90% success rate).
8. Lenticular sclerosis which is a common sign of aging. This is a result of lens fiber compression –> degeneration –> translucency.

Question 79

Topic: Entropion vs Ectropion

1. Define both terms.
2. What are the consequences of both conditions, respectively.
3. How are both of these conditions treated?

Answer 79

1. Entropion is the turning in of the edges of the eyelid so that the eyelashes and fur rub against the eye surface. Ectropion is a slack eyelid edge that is turned out, usually with a large notch or “crack” in the eyelid. It occurs mainly in larger dog breeds and is usually associated with excessively long eyelids (Bloodhound, Bullmastiff, Great Dane, Newfoundland, Saint Bernard, and several Spaniel breeds).
2. • Entropion: conjunctival and corneal irritation, and if protracted, corneal scarring, pigmentation, and corneal ulceration
   • Ectropion: Conjunctival exposure to environmental irritants and secondary bacterial infection can result in chronic or recurrent conjunctivitis.
3. Early spastic Entropion = Temporary eyelid-tacking sutures or surgical staples left in place for 2–3 weeks may be used. Established entropion = requires surgical correction that, in breeds with heavy upper facial folds (such as the Chinese Shar-Pei), may need to include tacking of the dorsal facial folds to achieve optimal results.

Ectropion:
- Topical anti-inflammatory medications may temporarily control mild or intermittent inflammation.
- Mild cases may also be controlled by repeated, periodic lavage with eyewash and chronic lubrication with topical gel or ointment.
- Generally, surgical eyelid-shortening procedures are indicated to provide more normal eyelid function and more appropriate protection of the globe.

Question 80

Topic: Uveitis
1. Define uveitis.
2. Describe the pathogenesis.
3. List the causes of uveitis.
2. List the major clinical signs
2. How do you diagnose uveitis?
3. How is this tx?

Answer 80

1. Uveitis is inflammation of the deep tissues of the eye.
2. Leaky vessels within the iris, the colored portion of the eye.
3. In all species, the cause is usuallly idiopathic.
   - Unilateral uveitis: Penetrating and non-penetrating trauma, rarely intraocular neoplasms or helminths.
   - Bilateral uveitis: immune mediated and infectious diseases including = FIP, FeLV, FIV, Feline Toxoplasmosis, Systemic mycoses in dogs and cats, Canine brucellosis, Canine Ehrlichiosis Leptospirosis in horses, Bovine MCF, IBR, EVA, CSF.
4. Conjunctival hyperemia, photophobia, blepharospasm, aqueous flare (cloudiness of aqueous humor), color change of iris, midrange to miotic pupils.
5. Tonometry: IOP < 10 mmHg, BW to look for underlying cause
6. Topical or systemic corticosteroids or NSAIDs unless secondary to protozoal or fungal infection or corneal ulceration, topical atropine for pain, treat underlying cause.

Question 81

What is distichiasis? How is it treated?

Answer 81

When the eyelashes grow out of the meibomian gland along the eyelid margin. This condition is only treated if there is corneal/conjunctival disease. Treatment involves destroying the follicular base of the eyelids via cryotherapy.

Question 82

What is ectopic cilia?

Answer 82

This is a condition in which eyelashes grow out of the meibomian gland and subsequently protrude through the conjunctival surface –> corneal irritation. Tx via excision, cautery, or cryotherapy.

Question 83

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 83

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 84

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 84

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 85

How do flea adulticides work?

Answer 85

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 86

How do insect growth regulators work? Give examples.

Answer 86

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

Question 87

What flea repellent repels via physical contact?

Answer 87

Permethrin; toxic to cats

Question 88

What is the etiology of Zinc Responsive Dermatosis in dogs?

Answer 88

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 89

Topic: Discoid Lupus Erythematosus (DLE) in dogs

1. What are the c/s?

Answer 89

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 90

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 91

What type of medication is Firocoxib?

Answer 91

An NSAID; do not give with steroid

Question 92

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 93

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 94

Topic: Sarcoptic Mange

1. What is the etiologic agent of this disease?
2. What are the clinical signs?
3. How is this disease diagnosed?
   4.How is this disease treated?
4. Is this disease zoonotic?

Answer 94

1. Sarcoptes scabiei canis
2. A. Intense pruritus
   B. Small bumps
   C. Excoriations, crusts, and seborrhea on abdomen, chest, ears, elbows, and legs
3. Skin scrapings
4. A. Lime-sulfur dips
   B. Selamectin
   C. Single dose of fl uralaner
   D. Ivermectin is effective, however is toxic in breeds that have the MDR1 mutation (e.g., collies)
5. It is zoonotic, however disease is self-limiting in humans

Question 95

What parasite is pictured below?

Answer 95

Sarcoptes scabei canis

Question 96

Topic: Demodex Mange

1. What is the etiologic agent?
2. Where can these mites be found?
3. How is it diagnosed?
4. How is demodex mange treated?

Answer 96

1. Demodex canis
2. In the hair follicle and sebaceous glands
3. deep skin scrapings or hair plucking
4. A. macrocyclic lactones
   B. milbemycin oxime
   C. moxidectin, ivermectin
   D. isoxazolines

Question 97

Topic: Cheyletiellosis (walking dandruff)

1. What is the etiologic agent of this disease?
2. What are the clinical signs?
3. How is it diagnosed?
4. How is this disease treated?

Answer 97

1. Cheyletiella yasguri
2. A. Intense pruritus (but sometimes no itching)
   B. Scaling on the back
   C. “Dandruff” that moves around on the animal’s fur
3. Direct observation and microscopy
4. A. Lime-sulfur dips
   B. Selamectin
   C. Single dose of fluralaner
   D. Ivermectin is effective, however is toxic in breeds that have the MDR1 mutation (e.g., collies)

Question 98

What parasite is pictured below?

Answer 98

Cheyletiella yasguri

Question 99

Topic: Canine Familial Dermatomyositis

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

Answer 99

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

Question 100

Topic: Proptosis

1. Define proptosis. What happens as a result?
2. What is the most common cause of proptosis?
3. How is this treated?
4. What is the prognosis?
5. What are some complications of this disease?

Answer 100

1. Proptosis is anterior displacement of the globe and the eyelids become trapped behind the globe. This leads to secondary orbital hemorrhage,, swelling, and corneoconjunctival drying and ulceration.
2. Proptosis is most commonly caused by blunt trauma such as getting hit by a car, fighting with another animal, etc.
3. A. Lubricate the exposed cornea and conjunctiva.
   B. Surgery: Lateral canthotomy (cut lateral canthus of eye to relieve pressure) + complete temporary tarsorrhapy (closing eyelids together; two interrupted horizontal mattress sutures with stent).
   B1. Post op systemic and topical AB, corticosteroids, +/- mydriatics
4. Prognosis depends on pupil size and reflexes, duration of exposure, breed (brachys are predisposed), other systemic trauma.
5. KCS, corneal ulceration, blindness due to optic nerve degeneration, lateral strabismus if medial rectus muscle is injured.

Question 101

Topic: Cherry Eye

1. Define Cherry eye
2. What is the common signalment of this condition?
3. How is this typically treated?
4. What are some complications if this is not treated?

Answer 101

1. Cherry eye is hypertrophy, inflammation, and subsequent prolapse of the nictating membrane.
2. Beagles, Bulldogs, Boston terrier, cocker spaniel, etc.
3. Surgical replacement. Partial or complete excision should be avoided as this predisposes the patient to KCS.
4. Increased risk of developing KCS; Even if replaced the dogs are still at risk of developing KCS. Monitor tear production of these dogs after surgery.

Question 102

Topic: Canine Hypertrophic Osteodystrophy

1. What is the current theory on the cause of this condition? Is there a breed predisposition?
2. What is seen clinically in these patients?
3. What diagnostic tests would you run? What would you see diagnostically?
4. Is there any treatment?
5. What is the prognosis?

Answer 102

1. Weimaraners are predisposed and litter-mates will commonly be affected. Although the exact cause is unknown, the leading hypothesis is recent vaccination leading to hyper-reactivity of the immune system. In a study of 53 Weimaraners with HOD, all had been vaccinated within the past 30 days.
2. Clinically you will see a painful, swollen, warm distal limb. Pain is elicited upon metaphyseal palpation.
3. Radiographs - double physeal line
4. Analgesics
5. Prognosis is excellent although the patient may experience flare ups.

Question 103

Topic: Canine Panosteitis

1. List the clinical signs seen in this condition. What is seen on physical exam? Is there a breed disposition?
2. What diagnostic tests would you run? What do you see?
3. How is this condition treated?
4. What is the prognosis?

Answer 103

1. Typically seen in young large and giant breed dogs; more common in males. Will be pyrexic, acutely lame, painful on long bone palpation (femur, humerus).
2. Increased medullary opacity in long bones, periosteal new bone
3. Analgesics
4. Prognosis is excellent although the patient may experience flare ups.

Question 104

Topic: Legge-Perthes Disease

1. Define this condition.
2. What is the typical signalment?
3. What will you see on exam?
4. What diagnostic tests would you run? What do you see?
5. How is this condition treated?
6. What is the prognosis?

Answer 104

1. Avascular necrosis of the femoral head
2. 3-12 mo old small or toy breed dogs.
3. Pelvic limb lameness
4. Radiographs: moth eaten appearance of the femoral head and neck, decrease bone opacity at femoral epiphysis.
5. FHO or total hip replacement, analgesics
6. Prognosis with surgery is good to excellent

Question 105

Topic: Patellar Luxation

1. What is this condition caused by?
2. Describe the pathogenesis.
3. How is this condition diagnosed ?
4. How is this condition treated?
5. What is the prognosis?

Answer 105

1. Hereditary disorder
2. Ectopic development of the patella medial or lateral to the trochlear groove of the femur

Patellar luxation can be classified according to the level of severity:

Grade I — Clinical signs are mild and infrequent, and the patella can be manually luxated but easily returns to the trochlear groove.

Grade II — The patella luxates during flexion of the joint and is repositioned during extension, causing animals to have a resolvable skipping lameness.

Grade III — the dislocated patella is more frequently out of, instead of in, the trochlear groove, and lameness is consistent. Bone deformities are evident in these animals.

Grade IV — Lameness and limb deformations are most severe.

3. Xrays, ortho exam
4. Surgery
   - varies based on severity of condition
   - can be as simple as a fascial releasing incision to deepening the trochlear groove, tibial crest transposition, etc.
5. Prognosis is good in mild or moderately affected patients.

Question 106

Topic: Osteoarthritis

1. Unlike in humans, OA can begin? What is the typical signalment?
2. OA development depends on?
3. This disease is characterized by?
4. What is a key clinical sign of OA?
5. How is this disease diagnosed?
6. How is this disease treated?

Answer 106

1. Early on in life. In dogs, usually seen in German Shepherd Dog, Labrador Retriever. In cats, it is usually seen in Maine Coons since they are prediposed to developing hip dysplasia.
2. Heritable abnormalities such as elbow dysplasia (OCD, UAP, FMCP), angular limb deformities, etc).
3. A. Hyaline cartilage clefts and thinning
   B. Joint effusion
   C. Periarticular osteophyte formation
4. Lameness, difficulty rising, difficulty going up and down stairs, limited jumping and playing.
5. Xrays
6. Weight loss, controlled exercise, fatty acid supplementation, NSAID therapy, chondroprotectants such as glucosamine (support cartilage repair), acupuncture, laser therapy, +/- surgery (arthrodesis, joint replacement, etc).

Question 107

Topic: Exocrine Pancreatic Insufficiency

1. Most common in what dog breeds?
2. Describe the pathophysiology of this disease.
3. What is the most common cause in dogs?
4. What is the most common cause in cats?
5. What is a common sequela of this disease?
6. What are the KEY clinical signs?
7. What diagnostic tests do you run?
8. How is this condition treated?

Answer 107

1. German Shepherds, Collies and English Setters
2. Inadequate synthesis and secretion
   of digestive enzymes by the exocrine pancreas –> inactivity of digestive enzymes in the lumen of the small intestine.
3. The most common cause of EPI in dogs is pancreatic acinary atrophy.
4. The most common cause of EPI in cats is pancreatitis.
5. Malassimilation of nutrients (fats, carbs, proteins, vitamins, trace elements) + SIBO
6. Polyphagia, diarrhea and weight loss in a young animal
7. A. BW is usually normal
   B. Trypsin-like immunoreactivity or pancreatic lipase immunoreactivity is low (< 5 ug/l)
8. A. Exogenous pancreatic enzyme supplementation is the cornerstone of treatment of canine and
   feline EPI.
   - Powdered pancreatic extracts are usually adequate
   B. Parenteral cobalamin, vitamin K and oral vitamin E supplementation
   C. Highly digestible, low-fiber diet

The correct answer is pancreatic acinar atrophy. This is an idiopathic condition where the exocrine cells of the pancreas atrophy with minimal inflammation. Chronic pancreatitis is a much more common cause of EPI in cats than dogs. For this reason, dogs with EPI do not usually have concurrent diabetes mellitus because the endocrine cells are spared, whereas cats often do have concurrent DM. Neoplasia and infection are rare causes of EPI.

Question 108

Topic: Canine & Feline Pancreatitis

1. Describe the etiology of this condition.
2. List the clinical signs seen in dogs and cats. What about the c/s for severe necrotizing pancreatitis?
3. How is this condition diagnosed?
4. How is this condition treated?

Answer 108

1. Canine pancreatitis is almost always sterile. The etiology is not known, but these risk factors should raise your suspicion:
   ● Fat – obesity, fatty meals, hyperlipidemia
   ● Systemic inflammation, trauma, ischemia
   ● Endocrine diseases – hyperadrenocorticism, diabetes mellitus
   ● Drugs – azathioprine, l-asparaginase, tetracycline, doxorubicin
   ● In cats, the causes of pancreatitis are not as well understood
2. –> Dogs
   ● Mainly GI signs: vomiting, diarrhea, anorexia, cranial abdominal pain. A dog that hunches in a “praying posture” is a diagnostic clue for pancreatitis.
   ● Severe necrotizing pancreatitis can cause hypovolemia, fever, tachycardia, jaundice, and the systemic inflammatory response syndrome (SIRS).

–> Cats
● Tend to have non-specific lethargy and anorexia and may or may not have any of the other GI signs listed above for dogs.

3. A. BW: Serum amylase and lipase are nonspecific and unreliable but may be markedly elevated.
   B. Imaging: AUS
   C. cPLI or fPLI - most SENSITIVE TEST
4. –> Dogs:
   A. Delay feeding OR post-duodenal feeding by tube, and/or feeding a NO fat diet
   B. IVF
   C. H2 blockers (i.e. Ranitidine) and anti-emetics
   D. Analgesics
   –> Severe Pancreatitis:
   A. Antibiotics are only indicated if pancreatic necrosis or sepsis is suspected
   B. +/- Plasma or heparin administration
   –> Chronic Pancreatitis
   A. Low fat, highly digestible diet

–> Cats:
A. Pain management
B. Antiemetics
C. Antibiotics
D. H2 Blockers
E. Treat underlying disease

Question 109

Topic: Urolithiasis

1. What are the most common types of urinary stones in dogs and cats?
2. Medical dissolution is possible for what stones?
3. Which urinary bladder stones are radioLUSCENT?
4. What type of diets should be used for urinary stones?
5. What are the general management considerations for all stone types?

Answer 109

1. Struvite and Calcium Oxalate
2. Medical dissolution is possible for most stones except calcium oxalate.
3. Cystine and urate stones are and therefore may NOT be visible on radiographs.
4. An alkalinizing diet should be used for cystine and urate stones. A reduced protein diet should be used for cystine, urate, canine struvite, and to a lesser degree calcium oxalate stones.
5. A. Increase urine volume by providing a diet with high moisture content.
   B. Reduce the quantities of crystal-forming substrates.
   C. Increase urinary solubility of crystal forming substrates via ph change.

Question 110

Topic: Urolithiasis

What is the main treatment option for dogs suffering from urate bladder stones? Is there a breed predisposition?

Answer 110

The main treatment option is alkalizing the diet and allopurinol.

Allopurinol will reduce the amount of uric acid produced, but the patient must be closely monitored for the formation of Xanthine stones.

Urate are formed from diets high in protein which are metabolized to uric acid, acidifying the urine. The dalmatian breed is highly predisposed to the formation of urate stones.

Question 111

Topic: Struvite Urolithiasis

1. What are struvite urine stones composed of?
2. In dogs, struvite stones are usually associated with? In cats?
3. How do we treat struvite urolithiasis?

Answer 111

1. Magnesium, ammonium, phosphate
2. Urinary tract infections caused by urease positive microbes. In cats, struvite stones are sterile.
3. A. Antibiotics based on urine culture and sensitivity.
   B. Struvite stones thrive in an alkaline environment so we want to acidifiy the diet. Additionally, we want to give high quality, low protein diet to reduce the amt of urease.
   - Low magnesium, phosphate, and ammonium diet. Decreased protein –> decreased urea –> less ammonia produced by the enzyme urease. This is important for dogs especially because of the urease positive microbes.

Question 112

Topic: Canine urolithiasis
What are the main treatment options for cystine stones?

Answer 112

1. Reduced protein, sodium restricted, urine alkalinizing diet.
2. Urine alkalinizer (potassium citrate (preferred), or oral sodium bicarbonate)
3. Cuprimine and 2-MPG (binds to cystine to form a more soluble compound) are treatments used for cystine stones.

Question 113

Topic: Canine urolithiasis

1. What breeds are prediposed to developing calcium oxalate stones?
2. How is this treated?
3. How can these be prevented?

Answer 113

1. Schnauzers, Lhasa apso, Yorkies, Bichon Frise, Shih Tzu, Mini poodle
2. These are the most difficult stones to treat; typically require surgical removal, voiding hydropulsion, or lithotripsy.
3. Provide an alkalinizing diet to prevent new stones from forming!
   A. Low sodium diet: high sodium intake increases urinary calcium. Also, low protein, Ca, oxalate, Vit D, sodium.
   B. Adequate phosphorous concentration to prevent Vitamin D activation. Also, magnesium, Vit B6.

Question 114

Topic: Systemic Mycoses

What part of the U.S. can the following fungi be found?

1. Coccidiomycosis
2. Histoplasmosis
3. Blastomycosis
4. C. gatti cryptococcosis

Answer 114

1. AKA VALLEY FEVER; Arizona, California, Nevada, and New Mexico
2. Midwest and Mississippi river valley
3. Ohio River Valley (east of the Mississippi River)
4. Washington, Oregon, California

Question 115

Topic: Systemic Mycoses - Histoplasmosis

1. What species are most commonly affected?
2. How is it transmitted?
3. Describe the life cycle.
4. What is seen clinically in these patients?
5. How is this disease diagnosed?
6. How is this treated?
7. How can you tell that patient’s prognosis is improving?

Answer 115

1. Dogs, cats
2. Can be found in the soil; distributed by bird and bat feces
3. Inhaled -> converted to yeast and replicated in lungs -> moves inside blood cells -> circulates throughout body
4. –> Dogs:
   ■ GI: Weight loss, bloody stool, diarrhea (dogs > cats)
   ■ Respiratory: Cough, breathing difficulty, increased RR
   ■ Other organs can be affected as well (Nodular skin lesions, joint swelling etc.)
   –> Cats
   ■ Respiratory: Cough, breathing difficulty, increased RR
   ■ Weight loss and anorexia (No bloody stool)
   ■ Other organs can be affected as well (Nodular skin lesions, joint swelling etc.)
5. A. CBC: Anemia, neutrophilic leukocytosis, thrombocytopenia
   B. Chemistry: Hypoalbuminemia, hypercalcemia possible
   C. Radiographs: Diffuse or linear, nodular interstitial pattern, hilar lymphadenopathy, pleural effusion
   D. Fungal culture: Dangerous due to infectious aerosolization to lab workers
   E. Antigen testing: Serum, CSF or urine

6.
A. Itraconazole: for 4-6 mo or at least 1 mo post c/s
- Side effects: Anorexia, diarrhea, vomiting, hepatic enzyme elevations, vasculitis
- Recheck monthly to monitor liver values

7. Decline in antigen concentration after 1-2 months of treatment is a good sign

Question 116

Topic: Systemic Mycoses - Blastomycosis

1. What species are most commonly affected?
2. How is it transmitted?
3. Describe the life cycle.
4. What is seen clinically in these patients?
5. How is this disease diagnosed?
6. How is this treated?
7. How can you tell that patient’s prognosis is improving?

Answer 116

1. Dogs and cats; think hunting dog
2. Soil fungus – in decaying vegetation, pigeon and bat feces
3. Inhaled -> converted to yeast and replicated in lungs -> moves inside blood cells -> circulates throughout body
4. stays in lungs more than other fungi but can also invade other body
   systems
   ○ Cough, increased RR, increased effort
   ○ Lethargy, anorexia and weight loss
   ○ Lymph node enlargement
   ○ Other body systems
   ■ Bone infection: Lameness
   ■ Urinary tract: Bloody urine
   ■ Eye: Light sensitivity, pain, glaucoma
   ■ Skin: Draining tracts, proliferative lesions, purulent material
5. Chest radiographs: a bronchointerstitial “snowstorm” pattern of pneumonia likely in hilar areas
   ○ Impression smear of cutaneous lesion or of draining tract -> Very thick-walled budding yeast
   ○ CBC: Chronic inflammation – mild anemia, monocytosis, lymphopenia, eosinophilia
   ○ Chemistry: Hypoalbuminemia, hyperglobulinemia
   ○ Urinary antigen test or PCR
6. Itraconazole for at least 2-3 mo and continue for 1-2 mo post c/s
   - Side effects: Anorexia, diarrhea, vomiting, hepatic enzyme elevations, vasculitis
   - Recheck every month to monitor liver values
7. Decline in urine antigen concentration after 1-2 months of treatment is a good sign

Question 117

Topic: Systemic Mycoses - Crpytococcus

1. What species are most commonly affected?
2. How is it transmitted?
3. Describe the life cycle.
4. What is seen clinically in these patients?
5. How is this disease diagnosed?
6. How is this treated?
7. How can you tell that patient’s prognosis is improving?

Answer 117

1. Cats more susceptible than dogs; dogs likely have more severe disease
2. Transmission is through pigeon poop, soil
3. Inhaled -> spread by macrophages in the bloodstream to organs
4. Respiratory – sneezing, nasal discharge (mucoid or hemorrhagic)
   ○ Weight loss, lethargy, anorexia
   ○ Ocular changes
   ○ Neurologic abnormalities
   ○ Cutaneous lesions more likely in cats
   ■ Roman nose presentation (swelling of bridge of the nose)
5. CBC: nonspecific – nonregenerative anemia, leukocytosis
   ○ Chemistry: changes reflect whichever organ is involved
   ○ Cytology: round, purple/blue with thick capsule
   ○ Serology
6. Amphotericin B +/- fluconazole for 3-5 mo to a year and for 2 mo post c/s
   - Side effects: nephrotoxicity, vomiting, anorexia
   - Must monitor kidney values (and hepatic values if on -azole
7. Monitor with latex agglutination antigen test to evaluate response to treatment

Question 118

Topic: Systemic Mycoses - Coccidiomycosis

1. What species are most commonly affected?
2. How is it transmitted?
3. Describe the life cycle.
4. What is seen clinically in these patients?
5. How is this disease diagnosed?
6. How is this treated?
7. How can you tell that patient’s prognosis is improving?

Answer 118

1. Cats and dogs affected
2. after heavy rainfall, dust storms or earthquakes spores come to surface and inhaled
3. Inhaled -> lymphatic dissemination to organs
4. Cough, increased respiratory effort
   ○ Weight loss/lethargy/weakness
   ○ Lymphadenopathy
   ○ Seizures
   ○ Lameness/bone pain
   ○ Uveitis/blindness
5. CBC: Nonregenerative anemia, neutrophilia
   ○ Chemistry: Hypoalbuminemia, hyperglobulinemia, if liver is involved -> elevated liver enzymes, if the kidneys are involved -> BUN and phosphorus increases
   ○ Radiographs: Diffuse, interstitial or mixed alveolar pattern, most will have hilar lymphadenopathy
   ○ If draining tracts, impression smears may reveal spherules with double walls and full of endospores
   ○ Serology
   ○ Culture only in a special lab.
6. Ketoconazsole, Itraconazole for at least 3 mo and 2 mo post c/s. Can add Amphotericin B is not responding to tx.
   - Side effects: Anorexia, hepatic enzyme elevations, adrenal insufficiency,
   cataracts (with >12 months therapy)

Question 119

Topic: Foreign body obstruction

1. What are the clinical signs of a FBO?
2. What diagnostics should you run ? What do you see?
3. How is this condition treated?
4. If you have to perform a resection and anastomosis procedure on a foreign body obstruction patient, what risk are you most afraid of within the first 3 to 5 days postoperatively and why?

Answer 119

1. Clinical signs include vomiting, anorexia, pain on abdominal palpation, diarrhea.
2. A. Xrays - you will see multiple distended loops of intestine (gas filled)
   B. AUS
   C. +/- contrast rads with barium
   D. Bloodwork - electrolyte imbalance, acid base abnormalities; Hypochloremia such as
3. A. Surgical removal (Enterotomy + removal) +/- resection and anastomosis (depends on health and viability of intestine)
   B. Correct electrolyte +/- acid-bace imbalance
   C. Post-op AB - Cefazolin if enterotomy of stomach and proximal intestine, Cefoxitin for lower SI and colon.
4. Your biggest concern is septic peritonitis due to leakage at the incision site. This can occur if fibrin degrades at the incision site before proper college and deposition. The most common time for this procedure to fail is within the first 3 to 5 days.

Question 120

Topic: Coccidiosis

1. What is the most common coccidia of cats and dogs?
2. What age range is most commonly affected?
3. What is the most common c/s?
4. How is this disease diagnosed?
5. How is this condition treated?
6. How can this condition be prevented?
7. Is this a disease of zoonotic concern?

Answer 120

1. Isospora spp.
2. Young puppies and kittens (4-12 weeks) in highly populated and contaminated areas.
3. Diarrhea
4. Fecal flotation
5. Sulfonamides such as Sulfadimethoxine or trimethoprim sulfa.
6. Maintain a clean environment; organism is highly environmentally resistant so need to use chlorine to disinfect.
   - It is important to pick up the stools as soon as possible to avoid sporulation and contamination of the environment with cysts.
7. Luckily, Isospora is species-specific so zoonosis is not a concern.

Question 121

Topic: Horner’s Syndrome

1. Define Horner’s Syndrome.
2. What are the clinical signs?
3. How can you diagnose and confirm that you are dealing with horner’s syndrome?

Answer 121

1. Horner’s syndrome occurs secondary to either a) trauma to the brachial plexus, thorax, or neck, b) otitis media/interna, c) guttural pouch disease in horses, or d) a lesion at in the hypothalamus, T1-3, or the cranial cervical ganglion (most common form of Horner’s).
2. C/S include miosis, ptsosis, and enopthalmos.

Question 122

Topic: Giardiasis
1. What is the etiology of giardia? Which of these are zoonotic?
2. What is the classic case in dogs and cats?
3. How is this disease transmitted?
4. What species is the most important reservoir?
5. Is this a reportable disease?
6. How is this disease diagnosed?
7. How is this disease treated?

Answer 122

1. Giardia duodenalis/intestinalis
2. Giardia A and B are zoonotic, the others are host specific
3. Weight loss, chronic greasy diarrhea (usually no blood).
   - May present asymptomatic
4. Fecal-oral transmission, fomites, drinking untreated water from wells/lake water, eating contaminated food.
   - The type of giardia that infects dogs and cats does not infect humans. The giardia that infects dogs does not infect cats and vice versa.
5. Humans
6. In humans it is!
7. Fecal examination of the trophozoite; Giardia should be distinguishable from trichomonads which have a single nucleus and an undulating membrane.
8. Fenbendazole, metronidazole.

Question 123

Topic: Sarcoptic Mange

1. What is the etiology?
2. What are the clinical signs?
3. How is it diagnosed?
4. How is it treated?

Answer 123

1. Sarcoptes scabei
2. A. Intense pruritus
   B. Small bumps, excoriations, crusts, and seborrhea on abdomen, chest, ears, elbows, and legs
3. A. Skin scraping
   B. Positive pinnal-pedal reflex
4. A. Lime-sulfur dips
   B. Selamectin
   C. Fluralaner - not labeled
   D. Ivermectin but not in collies

Question 124

Topic: Otodectic Mange

1. What is the etiology?

Answer 124

1. Otodectes cynotis

Question 125

Topic: Demodex Mange

1.Etiology?
2. Pathogenesis and c/s
3. How is this diagnosed?

Answer 125

1. Demodex canis
2. There are 2 clinical forms of canine demodicosis: Localized (limited to a small area) and generalized (found on the entire body).
   A. Localized demodicosis is usually seen in dogs less than 1 year old. Affected dogs will have 1 to 5 small, isolated areas that are usually hairless, red, and scaly.
   B. The generalized form of demodicosis can occur in young dogs (juvenile-onset) or in adults (adult-onset). Affected dogs have severe disease with widespread inflammation of the skin.
   - Juvenile-onset generalized demodicosis is the result of an inherited immune system defect.
   - Adult-onset generalized demodicosis is often associated with an underlying disease that has suppressed the immune system (such as cancer, Cushing disease, hypothyroidism, or diabetes).
   - Both types of generalized demodicosis can cause hair loss, reddened and swollen skin, increased pigmentation (darkening of the skin), raised lumps that look like acne, and scabs. Secondary bacterial infections (pyodemodicosis) are common.
3. Deep skin scrapings
4. A. Spot tx: Moxidectin + Imidacloprid
   B. Ivermectin, milbemycin oxime, or fluralaner

Question 126

Topic: Chocolate Toxicity
1. What toxic metabolites are in chocolate?
2. What are the c/s?
3. How is this treated?

Answer 126

1. methylxanthines, theobromine, and caffeine; The darker the chocolate, the higher the concentration of toxins
2. Signs start in 6-12 h and last up to 72 h in severe cases:
   A. Low dose: vomiting, diarrhea, restlessness, polydipsia
   B. High dose: agitation, ataxia, tremors, tachycardia, and ventricular premature contractions (VPCs)
   C. Very high dose: seizures, hyperthermia, cardiovascular decompensation, coma, death
   –> Pancreatitis a risk w/in a few days from fat content in chocolate
3. A. Emesis and AC if recent, repeated AC w/ ongoing clinical signs
   B. IV fluids and Tx GI signs
   C. Methocarbamol for tremors, diazepam for seizures
   D. Anti-arrhythmogenics to control VPCs and other arrhythmias
   E. Monitor ECG, BP, acid-base, and electrolytes (hypokalemia possible)

Question 127

Topic: Xylitol Toxicity
1. What is the pathogenesis?
2. How is this diagnosed?
3. How is this treated?

Answer 127

1. A. Hypoglycemia: onset at 30 m to 18 h depending on product ingested; vomiting, weakness, ataxia, seizures
   B. Liver failure: 1-2 d w/ higher dose exposure; vomiting, depression, icterus, coagulopathy
2. A.Liver failure w/ hyperbilirubinemia, prolonged clotting times
   B. Hyperphosphatemia (poor prognostic indicator)
3. A. Early emesis, no AC
   B. IV fluids w/ dextrose (hypoglycemia can last 24 h)
   C. Frequent BG checks
   D. Liver enzyme monitoring q24h x 3 d
   E. Heptatopretactants (e.g., N-acetylcysteine, S- adenosylmethionine, silymarin)
   F. Transfusions (plasma +/- whole blood) for coagulopathies

Question 128

Topic: Grape Toxicity

1. What is the pathogenesis?
2. What are the clinical signs?
3. How is this disease diagnosed?
4. How is it treated?

Answer 128

1. Tartaric acid in grapes causes renal damage
2. A. First 12-24 h (acute): minimal signs, occasionally vomiting/diarrhea
   B. 24-72 h post-ingestion (subacute)
   Vomiting, diarrhea, abdominal pain Dehydration PU/PD +/- subsequent decreased urine output
3. A. Acute: no bloodwork changes
   B. Subacute: azotemia +/- hypercalcemia, hyperphosphatemia, SG < 1/030 w/ casts in sediment
   C. Late stage: anuria, worsening azotemia and hyperkalemia
4. A. Emesis + activated charcoal (AC): ideally w/in 6 h, but up to 12 h post-ingestion
   B. Fluid diuresis x 48 h, longer if azotemic
   C. Recheck renal values, electrolytes q24h x 3 d
   D. Anuric failure: rehydrate and consider furosemide, mannitol, or dopamine; +/- hemodialysis
   E. Symptomatic treatment for GI upset: antiemetics, antacids, antidiarrheals

Question 129

Topic: NSAIDs Toxicity

1. What is the difference in terms of c/s/damage done by ibuprofen vs aspirin?
2. What is seen on lab work for both respectively?
3. How is this treated?
4. What is the difference in pathogenesis between the two?

Answer 129

1. Ibuprofen causes renal damage. Aspirin causes hepatic disease.
2. A. Ibuprofen: anemia, low protein from GI ulcers, azotemia, tubular casts and proteinuria
   B. Aspirin: Anemia, low protein from GI ulcers, increased buccal mucosal bleeding times (indicating platelet dysfunction) w/ normal platelet count, metabolic acidosis, increased liver enzymes and hyperbilirubinemia
3. Emesis, IVF, GI protectants, blood transfusions, diazepam for seizuress, diuresis for renal damage
4. A. Aspirin: Major active metabolite is salicylic acid; inhibits platelet function for the life of the exposed platelets (thus most commonly used therapeutically as antithrombotic)

B. NSAIDS inhibit prostaglandins by blocking COX enzymes that are needed for normal kidney blood flow and generating GI mucosal barriers

Question 130

Topic: Lymphoma

1. What are the clinical signs?
2. How is this disease diagnosed?
3. How is this disease treated?
4. What is the prognosis?

Answer 130

1. A. Generalized lymphadenopathy
   B. Anorexia
   C. Vomiting
   D. Weight loss
   E. Dyspnea
2. A. Cytology: predominance of lymphoblasts; biopsy required for de finitive diagnosis and grading
   B. Stage with thoracic radiographs and abdominal ultrasonography
   C. Anemia, thrombocytopenia, neutropenia with bone marrow involvement
   D. Hypercalcemia
   E. Bone marrow aspirate
   F. Phenotype with fl ow cytometry or immunohistochemistry to determine if B or T cell
3. Chemotherapy with combination protocol is best
4. A. T cell lymphoma has poorer prognosis (“B is better”)
   B. Prednisone before chemotherapy will decrease response to chemotherapy
   C. Many dogs can achieve remission with chemotherapy

Question 131

Topic: Osteosarcoma

1. What are the clinical signs?
2. How is this disease diagnosed?
3. How is this disease treated?
4. What is the prognosis?

Answer 131

1. A. Large or giant breed, bimodal age incidence (1.5-2y then 7-9y)
   B. Chronic, progressive lameness (acute if pathologic fracture)
   C. Cough if pulmonary metastases present

2.
A. Radiography: bony lysis (moth-eaten) and periosteal bone formation
B. Thoracic radiographs: 3 views to detect metastatic disease
C. CBC, chem profile , UA to stage
D. Fine needle aspirate (FNA) or biopsy (best to confirm diagnosis)
E. CT for axial tumors and to help plan surgery or radiation therapy

3. A. Palliative care
   B. Amputation
   C. Radiation
   D. Chemotherapy for micrometastasis (doxorubricin, carboplatin)
4. A. 75% are appendicular; common locations are proximal humerus, distal radius, distal femur, and proximal tibia (“away from elbow, toward knee”)
   B. 90% of dogs will have clear thoracic radiographs at initial diagnosis, but most will develop mets later, even with amputation
   C. Survival is 4-12 months, elevated ALP associated with poorer prognosis

Question 132

Topic: Mast Cell

1. This is considered to be ?
2. What breeds are predisposed?
3. What do MCT release when they degranulate? What do they cause as a result?
4. What grading system is used? What does it evaluate?
5. This is nicknamed ?
6. How is this disease diagnosed?
7. How is this disease treated?

Answer 132

1. The most common dermal malignancy in dogs.
2. Boxers, pugs, Boston terriers, other brachycephalic breeds (MCTs they develop are less aggressive and low grade tumors).
3. Mast cell granules release histamine, heparin, proteases, and cytokines when they degranulate.
   A. May cause GI ulcers, bleeding, poor wound healing, anaphylactoid reactions (vasodilation,
   hypotension, collapse, etc.)
4. Patnaik system
   A. Evaluate cell differentiation, mitotic figures, and invasiveness in surrounding tissues
5. The “great pretender” as they can look and feel like anything from a skin plaque, nodule,
   rash, or lipoma.

6.
A. FNA; Grade can NOT be determined by cytology
B. Biopsy of mass; Occasionally required for diagnosis if FNA is non diagnostic. Required for grading
C. FNA or biopsy of regional LN
D. +/- AUS and Xrays if indicated for high risk of metastasis (LN, Liver, Spleen, and Thoracic LN)

7. If metastasis is not present:
   A. Sx: Excision with 2-3 cm lateral margins and 1 fascial plane deep
   B. +/- Adjuvant radiation therapy if complete margins are not obtained

If metastasis present:
A. Vinblastine, CCNU, or other alkylating agents

Supportive Care:
A. Prednisone
B. H1 Blocker: Diphenhydramine
C. H2 Blocker - Famotidine, Ranitidine

Tyrosine Kinase Inhibitor
A. Toceranib (Palladia): First FDA-approved drug for canine cancer in the United States. Works by Inhibiting aberrant cell signaling pathways found in MCTs.

Question 133

Topic: Mammary Tumors

1. What are the clinical signs?
2. How is this disease diagnosed?
3. How is this disease treated?
4. What is the prognosis?

Answer 133

1. A. Palpable mammary chain mass or ulceration
   B. Intact or late spayed female
2. A. Excisional biopsy and histopathology
   B. FNA of regional lymph nodes
   C. 3-view thoracic radiographs and abdominal ultrasonography to screen for metastatic disease
3. A. Surgery depends on size and location (lumpectomy, regional/simple mastectomy, radical mastectomy), but best if can excise with a minimum of 2-cm margins in all planes +/- Inguinal lymph node removal
   B. Adjuvant chemotherapy for gross metastasis or advanced stage
4. A. 50% benign, 50% malignant
   B. Multiple tumors are common as are multiple tumor types C. Poorer prognosis if > 3 cm, lymph node involvement, or distant metastasis
   D. Spaying after 2 yr does not decrease risk

Question 134

Topic: Hemangsiosarcoma

1. Define hemangiosarcoma. Describe its behavior.
2. What are the c/s?
3. How is it diagnosed?
4. How is it treated?
5. What is the prognosis?

Answer 134

1. Hemangiosarcoma (HSA) is the most common primary tumor of the spleen in dogs and leads to the formation of abnormal blood vessels which can rupture and bleed. This tumor can also be found in the liver,
   skin, and heart. HSA is aggressive both locally and has a high rate of metastasis.
2. A. Lethargy
   B. Difficulty rising
   C. Abdominal distension
   D. Sudden death
3. A. Xray - look for metastasis
   B. Splenectomy
   C. Biopsy + histopathology
4. Surgery followed by chemotherapy
   A. Chemotherapy is strongly recommended due the aggressiveness of HSA and the short survival time with surgery alone (1-3 months).
   - The chemotherapy of choice is doxorubicin.
5. A. Without surgery, most pets succumb to their disease within one
   month.
   B. With surgery alone, survival times range from 1 to 3 months.
   C. With the addition of chemotherapy dogs have a median survival time closer to 6 months.

Question 135

Tumors of the skin - see feline

Question 136

Topic: SCC - oral

Question 137

Topic: Melanoma - oral

Question 138

Topic: IVDD

1. List the etiologies of IVDD.
2. What are the clinical signs?
3. How is this condition diagnosed?
4. How is this condition treated?
5. What is the prognosis?

Answer 138

1. A. Hansen Type I (Chondrodystrophic breeds): AKA Disc extrusion - Nucleus pulposus extrudes through annulus fibrosus –> Spinal chord/nerve root compression.
   B. Hansen Type II (Non-chondrodystrophic breeds): AKA Disc protrusion - Annulus fibrosis bulges out –> Nucleus pulposus herniates within annulus fibrosis –> diffuse compression
   C. Hansen Type III: AKA Low volume, high velocity - concussive injury to spinal chord; occurs in any breed
2. A. Reluctance to walk/jump, paresis, ataxia, +/- paralysis
   B. Cervical damage: Low head carriage, tetraparesis
   C. Thoracolumbar: Arched back, paraparesis
   D. Perform full neuro exam
   3.
   A. Orthogonal spinal rads to r/o fracture, luxation, neoplasia
   B. CT, MRI, myelography
   - MRI > CT
3. A. Pain w/ no or mild neuro deficits: Strict cage rest x 4-6 w
   - Muscle relaxants (e.g., methocarbamol)
   - Analgesics (e.g., NSAIDs (preferred over steroids) and opioids)
   B. More severe deficits - Decompressive surgery
4. Presence of deep pain is the most important prognostic indicator

Question 139

Topic: Cervical Spondylomyelopathy

1. AKA?
2. What is the etiology of this disease?
3. What is the classic signalment? What are the clinical signs?
4. How is this condition diagnosed?
5. How is it treated?
6. What is the prognosis?

Answer 139

1. Wobbler’s Syndrome
2. A. Disc-associated: Congenital vertebral canal stenosis w/ later intervertebral disc extrusion
   B. Osseous-associated: Osseous malformation and osteoarthritis compress the spinal cord
3. Doberman (> 7 yrs) or Great Dane ( > 3 yrs)
   A. Chronic progressive hindlimb weakness and ataxia +/- forelimb involvement
   B. Increased extensor tone in all limbs
   C. Cervical pain
   D. If caudal-cervical lesion: proprioceptive ataxia and weakness more obvious in hindlimbs.
4. A. Spinal Rads
   B. MRI > CT with myelogram
5. A. Medical: Exercise restriction, steroids/ NSAIDs= 50% of cases improve
   B. Surgical: Best chance for neuro recovery - 80% of cases improve
6. Short term = good, Long term = poor
   A. Most dogs deteriorate w/in 3 y of Dx regardless of Tx
   B. Great Danes and Dobermans are largely overrepresented - likely genetic.

Question 140

Topic: Megaesophagus
1. What is the etiology of this condition?
2. What are the clinical signs?
3. How is this condition diagnosed?
4. How is it treated?
5. What is the prognosis?

Answer 140

1. A. Idiopathic
   B. Secondary to:
   - Myasthenia Gravis
   - Congenital: German Shepherd, Mini Schnauzer, Fox Terrier,
   - Vascular ring anomaly
   - Temporary due to drug: Ketamine, Xylazine
2. A. Regurgitation: undigested food and water (different from vomit)
   B. Coughing, drooling
   C. Weight loss
   D. +/- Weakness (if d/t myasthenia gravis, polyneuropathy or polymyopathy)
   E. +/- Pneumonia
3. A. Thoracic rads +/- contrast esophagram
   B. AC Receptor AB test
   C. ACTH stim
   D. T4 + Free T4
   E. Lead levels
   F. EMG/nerve conduction
4. A. Tx underlying condition
   B. Upright feeding
   C. Cisapride: to aid in gastric emptying and reduce esophageal reflux
   D. PPIs (pantoprazole, ompreazole) or H2 receptor blockers (famotidine, ranitidine)

Question 141

Topic: Myasthenia Gravis

1. What is the etiology of this disease? What is the signalment?
2. Describe the pathogenesis.
3. What are the clinical signs?
4. How is it diagnosed?
5. How is it treated?
6. What is the prognosis?

Answer 141

1-2 Myasthenia gravis is an autoimmune disease that is caused by the destruction of acetylcholine receptors in the body. This can be congenital, where the patient is born with less ACh receptors than normal - this is rare, or due to hypothyroidism, cancer, a thymoma, or idiopathic.
- Acquired MG: German Shepherds, Akitas, Lab Retrievers, Golden Retrievers, Newfoundlands, Scottish Terriers
- Congenital MG: Jack Russell Terriers, Springer Spaniels, Smooth Fox Terriers

3. Generalized muscle weakness after activity but improves with rest.
   - +/- focal muscle weakness
   - Regurgitation
   - Vocal changes
   - Difficulty swallowing
   - Inability to close eyelids
4. • ACh AB test
   • Tensilon test: if MG positive, will temporarily improve muscle strength
   • Xrays
5. A. Pyridostigmine bromide: prolongs ACh at the receptor
   B. +/- pred
   C. Elevated feedings
   D. Tx underlying condition
   E. +/- Sx
6. Depends on underlying cause
   - Some dogs can go into remission in a few months
   - Others may need life long treatment

Question 142

Topic: IMHA
1. Canids typically develop IMHA because of?
2. What are the clinical signs?
3. What is seen on bloodwork?
4. What are some complications of IMHA?
5. How is it treated?
6. What are some DDx?

Answer 142

1. Primary IMHA usually occurs in young to middle aged dogs (6-8 yr)
   A. Predispositions
   - Females
   - Cocker spaniels
   B. Can be idiopathic (> 60% of cases) or d/t drugs, neoplasia, infection, vaccine related.
2. Onset of acute:
   - Anorexia, lethargy
   - Tachypnea, weakness, collapse
   - Pale MM
   - Icterus in 50% of patients
   - Heart murmur, splenomegaly
   - Tachycardia, tachypnea
3. A. Regenerative anemia (IMHA is the most common cause of hemolytic anemia in dogs)
   B. Polychromasia is almost always present
   C. Spherocytes (abnormally shaped RBC) IN DOGS ONLY
   D. Saline test - dilute blood with saline –> autoagglutination
   E. Leukocytosis
   F. Thrombocytopenia
   G. Positive Coomb’s test
   H. Elevated ALT and bilirubin - Elevated liver enzymes due to severe anemia and hypoxia
4. A. Concurrent immune mediated thrombocytopenia (Evan’s Syndrome)
   B. DIC
   C. Thromboembolism common and often fatal (Spleen, pulmonary, liver)

5.
A. Immune suppression: prednisone = first line; cyclosporine, chlorambucil (cats) = second line; can combine two to reduce time on pred or get faster response
B. Adjuvant IVIg: Block Fc receptors on MQ from binding to RBC and destroying them so it does not treat the patients long term, but in giving transfusion, those RBC are spared for that time. May see anemia lessen and give us time to give blood transfusion and have prednisone do the work.
C. Clopidogrel or baby aspirin (acetylsalicylic acid)

6. A. Infectious = Rickettsia, Babesia, Mycoplasma, Cytaxuzoon
   B. Neoplasia = Lymphoma, malignant histiocytosis
   C. Toxins/Drugs = Zinc pennies made after 1982, onions, garlic, Cephalosporins, Sulfa AB

Question 143

Topic: Kennel Cough

1. AKA?
2. What are the etiologies of this disease?
3. What are the c/s?
4. How is this disease diagnosed?
5. How is this disease treated?
6. How is this prevented? What is the prognosis?

Answer 143

1. Infectious tracheobronchitis (URI)
2. Distemper, Bordatella bronchiseptica, canine influenza virus, canine adenovirus, canine parainfluenza virus.
3. Persistent, dry nonproductive or harsh cough followed by retching or gagging (cough inducible via tracheal or laryngeal palpation).
   A. +/- fever, anorexia, depression nasal dc, pneumonia, productive cough.
4. Xrays to rule out pneumonia or other causes of cough. Usually based on c/s.
   +/- PCR of nasal or pharyngeal swabs to rule out influenza.
5. Supportive care
   A. Avoid hospitalization if possible b/s highly contagious and kennel cough is self limiting anyway.
   B. If cough is nonproductive, give cough suppressant, +/- AB for severe cases.
6. Prevent via vaccination, proper hygiene. Good prognosis

Question 144

Topic: Vaginal Cytology

1. Determine what stage of estrous the canine patient is in based on the vaginal cytology pictured

Answer 144

A. Anestrus. There is low cellularity, and the vaginal epithelial cells are mostly parabasal. Original magnification, 200×; Romanowsky variant stain.

B. Late proestrus. The vaginal epithelial cells are mainly large intermediate cells. Few superficial cells, RBCs, and bacteria are also noted. Original magnification, 200×; Romanowsky variant stain.

C. Estrus. There is a predominance of superficial vaginal epithelial cells (full cornification) and clear background. Few bacteria are noted. Original magnification, 100×; Romanowsky variant stain.

D. Early diestrus. There are small intermediate and parabasal vaginal epithelial cells, bacteria, numerous neutrophils, and moderate debris. Two metestrum cells (asterisk) are evident. Original magnification, 200×; Romanowsky variant stain.

Question 145

Topic: Canine Estrous Cycle

1. Describe the stages of estrous.

Answer 145

1. Proestrus
   Estrogen is a hormone produced by the ovaries during proestrus and peaks one to two days before the next stage (estrus). The estrogen produced in this stage causes bloody vaginal discharge and swelling of the vulva (or external genitalia). Dogs will be attractive to and may demonstrate playful behavior with male dogs during this stage but are not yet receptive to breeding. This stage can last, on average, between six to eleven days.
2. Estrus
   Estrus begins when the female is receptive to breeding. Estrus generally starts with a surge in luteinizing hormone (LH) due to decreasing estrogen and increasing progesterone. These hormonal changes are what influence the female’s receptivity to breeding. The vaginal discharge may change to straw-colored, although many variations exist between individuals. Estrus usually lasts five to nine days but may vary between one and twenty days.
3. Diestrus
   Diestrus begins when the female no longer shows signs of estrus, such as standing to be mounted. It is characterized by an elevation in progesterone, which peaks 2-3 weeks after ovulation and then plateaus at that elevated level for 1-2 weeks before slowly decreasing over 10-30 days. Progesterone (the pregnancy maintenance hormone) will increase during this stage, whether a dog is pregnant or not. Diestrus ends when progesterone concentrations return to baseline. During this stage, female dogs will no longer be attractive to males, nor will they allow mating. The external genitalia is indistinguishable between diestrus and the next stage, anestrus.
4. Anestrus
   Anestrus is the stage a dog enters either at the end of her heat cycle or after having a litter. Progesterone levels remain low throughout this stage. There is a period post-partum or after a normal heat cycle where the uterus must undergo a process called involution. This process repairs the uterus to prepare for repeating the estrous cycle and requires about four months to complete.

Question 146

Topic: Breeding

Question 147

Topic: Dystocia

Answer 147

‣ Uteroverdin - Brown or green; acts as iron storage for pregnancy. If only see green pigment, what does this tell you? This area has been detached from the uterus which is why we see green discharge. If do not see anything coming out, this means animal will have a dystocia.
‣ When see puppies and a bit of green discharge = normal b/c detached from endometrium
‣ But if only see green pigment and no pup - bad (give her ten minutes to see what happens but if straining and nothing come out = bad

			‣ 220-240 bpm: typical heart rate before term
	‣ 180-200 bpm normal range on the whelping day; during Stage II parturition
	‣ 160-180 bpm: stress; mild hypoxia?
			‣ < 140-160 bpm: decreases postnatal survival --> dystocia --> ER

Question 148

Topic: Collapsing Trachea

1. Signalment
2. C/S
3. Dx
4. Treatment
5. Prognosis

Answer 148

1. Yorkie, Pomeranians, etc. All toy/small breed dogs
2. “Honking” cough followed by a retch exacerbated by exercise.
3. A. Xrays (this is a dynamic disease so may be difficult to catch
   B. Fluoroscopy (capture dynamic xray images in real time)
   C. Endoscopy
4. Medical:
   A. Short course of corticosteroids
   B. Cough suppressant
   C. +/- weight loss
   Surgical:
   A. Tracheal stent only if unresponsive to medical management

Question 149

Topic: Insulinoma

1. This is a tumor of ?
2. Describe the pathogenesis of this disease.
3. What are the major clinical signs?
4. Diagnostics
5. Tx
6. Complications
7. Prognosis

Answer 149

1. Beta cells
2. Normally, when glucose levels fall below 60 mg/dL the body induces a negative feedback mechanism to prevent the release of insulin. In a case of insulinoma, the tumor does not respond to this negative feedback mechanism and continues to release insulin leading to hypoglycemia.
3. Intermittent neuro signs, weakness, seizing, non-specific lethargy.
4. AUS, bile acids, basal cortisol to rule out addison’s, measure insulin and glucose levels, MRI/CT.
5. A. Diet: high fat, protein, complex carbs; multiple small meals to keep glucose stable.
   B. Glucocorticoids: start with lowest dose possible and only increase as necessary
   C. Diazoxide: prevents insulin release (VERY SEVERE GI SIDE EFFECTS)
   D. Surgery = TX OF CHOICE
6. Pancreatitis, diabetes mellitus
7. Short term = good, long term = poor; almost 100% metastasis

Question 150

Topic: Heartworm

1. Heartworm disease is transmitted by?
2. Adult heartworms can be as long as ? and can live for?
3. Where do they live in the body once they have grown into adult worms? What does this cause?
4. What are the c/s seen in dogs and cats?
5. How is this diagnosed?
6. How is this treated?
7. Prevention ?

Answer 150

1. L3 larvae Dirofilaria immitis are transmitted by mosquitos. The Wohlbachia bacteria has been identified in heartworms.
2. 15-30 cm long and can live for 3-5 years
3. Pulmonary artery and the right ventricle leading to right ventricular hypertrophy.
4. Dogs: Signs consistent with r-sided heart failure
   A. Exercise intolerance, cough, dyspnea, ascites
   Cats:
   A. Acute: Due to worms dying –> embolism and inflammation –> salivation, tachycardia, shock, neuro signs, etc.
   B. Chronic: heartworm associated respiratory disease –> asthma like symptoms + vomiting, anorexia, weight loss
5. A. Dogs:
   - Heartworm antigen test is the test of choice; Detects ADULT worms; False negatives d/t Ag/AB complex, no adult females, light parasite load
   - Modified Knott’s test = may detect microfilaria (less sensitive than antigen test)
   - Xray: right sided cardiac enlargement (reverse D appearance) +/- right atrium
   B. Cats:
   - Heartworm antigen test = false negatives from low worm burden or all male infections
   - Heartworm antibody test = exposure but not necessarily infection
   - Thoracic radiographs and/or echocardiography can provide a diagnosis in some cases
   NOTE: On echocardiogram, heartworms appear as a distinct “double lined echodensity”
6. A. Dogs: Multi step process
   - To prevent new infection or tx susceptible larvae/microfilaria = macrocytic lactone
   - Start 2 mo prio to adulticide
   - Tx Wohlbachia bacteria = Doxycycline for 30 days prior to adulticide
   - Tx adults with melarsomina
   - 3 dose protocol: IM once, wait 1 month, then 2 doses 24 hr apart.
   - strict exercise restriction during adulticide therapy course

B. Cats
- Treatment is usually symptomatic with a heartworm preventative, bronchodilators and/or corticosteroids until the worms die (2-3 year life span in cats).

Question 151

Topic: Idiopathic epilepsy
1. Signalment
2. Pathogenesis
3. Diagnostics
4. Treatment + side effects of medication
5. Prognosis

Answer 151

1. 6 mo to 6 yr; any breed, any age
2. A. Status epilepticus: One seizure lasting more than 5 minutes OR 2+ seizures with incomplete interictal recovery.
   B. Cluster seizures: 2+ seizures within 24 hrs
3. Dx of exclusion
4. A. Acute: IV diazepam OR midazolam, levetiracetam, or phenobarbital loading dose
   B. Chronic: Oral phenobarbital
   - Phenobarb side effects: PU/PD, polyphagia, hepatotoxicity
5. Normal lifespan, good quality of life

Question 152

Topic: Degenerative myelopathy
1. Signalment
2. Etiology
3. C/S
4. Diagnostics
5. Treatment
6. Prognosis

Answer 152

1. Older (onset at 8-14 yo), many pure breeds
   predisposed (German Shepherd is poster child)
2. Gene mutation causes SOD protein aggregates to accumulate in neurons
3. History of progressive hindlimb weakness, ataxia, and CP deficits
   A. Physical exam:
   - Early = Upper motor neuron signs in hindlimbs - Late = Lower motor neuron in hindlimbs progressing to forelimbs, end stage dysphagia, and respiratory dysfunction
4. Dx of exclusion
5. No tx at this time.
   A. Suggested Tx: Vitamin E, C, B supplementation, protease 12
   inhibitors
   B. Physical rehabilitation to maintain muscle mass, nursing care
6. Px: Poor long-term because progression inevitable

Question 153

Topic: Tick Borne Diseases

1. Etiology
2. C/S
3. Diagnostics
4. Treatment
5. Prevention

Answer 153

1. A. Ixodidae family: Hard ticks (commonly Amblyomma spp., Dermacentor spp., Ixodes spp.)
   B. Argasidae family: Soft ticks (Otobius spp.)
2. Fever, anorexia, lymphadenopathy, splenomegaly, polyarthritis, etc.
3. C/S, finding ticks on patient
4. Doxycyline if suffering from clinical illness
5. A. Removal with forceps or hemostats close to skin and slightly twist
   B. Fipronil
   C. Fluralaner
   - NOTE: Both fipronil and fluralaner are flea adulticides but DO NOTa prevent re-infestation.
   - FIPRONIL IS TOXIC TO RABBITS

Question 154

Topic: Canine Distemper Virus
1. Etiologic agent
2. Transmission
3. C/S
4. Dx
5. Tx
6. Prevention

Answer 154

1. Canine distemper virus (paramyxovirus)
2. Aerosol, direct contact, fomites.
3. • Optho: KCS, Chorioretinitis
   • Pyrexia, serous to mucopurulent nasal discharge, lethargy, anorexia, vomiting, diarrhea.
   • Neuro signs
4. A. CBC: Leukpenia, particularly lymphopenia, occurs early in systemic disease
   B. RT-PCR of conjunctival, vaginal, or buffy coat smear
   C. Quantitative RT-PCR can distinguish infection from vaccination
5. Supportive care
6. Vaccination starting at 6-16 weeks of age