VIN Class 4 - Canine Info Flashcards
(154 cards)
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?
- Most common in older dogs but can also be congenital (cretinism - rare).
- Hypothyroidism most commonly occurs in dogs due to lymphocytic thyroiditis (aka immune destruction of the thyroid gland).
- The most common cause of misdiagnosis is suppressed hypothalamic-pituitary stimulation of the thyroid due to illness (euthyroid sick syndrome).
- 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.
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?
- Weight gain, obesity, lethargy, alopecia (often bilaterally symmetric over the lateral trunk, tail, and ventral thorax)
- 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 - 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.
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? **
- 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.
- 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. - 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) - 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. - 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.
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?
- Signs of Cushing’s disease can come from ACTH secreting pituitary tumors, cortisol secreting adrenal tumors, or iatrogenic steroid administration.
- PU/PD, Panting, Polyphagia, Pendulous abdomen, Pyoderma and thin skin, Pigmentation and symmetrical alopecia
- 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
Topic: Hyperadrenocorticism (Cushing’s Syndrome)
5. Treatment
- 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.
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?
- Inadequate insulin production or insulin resistance.
- The key clinical signs in a healthy diabetic patient are:
- PU/PD
- Polyphagia
- Weight loss
- Recurrent infections
- Cataracts in dogs - The key clinical signs in a DKA patient are:
- Anorexia
- Vomiting
- Weakness
- BG > 500
- Severe metabolic acidosis - BG; Will see hyperglycemia (usually > 300)
- USG: Will see Glucosuria +/- ketonuria
- BW: Metabolic acidosis, elevated liver enzymes and cholesterol
- 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. - 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.
List the duration of action of each insulin type from shorted to longest for both canine and feline DM patients:
Regular < NPH < Lente < PZI < Glargine < Detemir
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?
- Enteritis in young, unvaccinated dogs.
- 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.
- Leukopenia, fever
- Severe, often bloody, diarrhea
- Vomiting, loss of appetite, lethargy, dehydration
- Diagnosis is based on history, c/s, and lab work (leukopenia)
- Confirmed with fecal parvovirus ELISA test
- 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. - Vaccination, Careful hygiene, Isolation of ill animals, Disinfection with bleach
Topic: Pyometra
- Define this condition.
- Most common signalment
- When does it typically occur? Explain why
- List the clinical signs
- How is this condition diagnosed?
- How is this condition treated?
- Pyometra is a bacterial infection of the uterus due to hormonal changes in unspayed dogs.
- It is reported primarily in dogs more than 5 years old.
- 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.
- 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.
- The infection is diagnosed by physical examination, determination of the nature of the discharge, ultrasonography, x-rays, and laboratory and blood tests.
- 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.
Topic: Congestive Heart Failure
- List the classic clinical signs seen in patients with CHF.
- What diagnostics would you run on a patient with possible CHF?
- How is CHF treated?
- What is the prognosis?
- Dypsnea, tachypnea, exercise intolerance, cough
- +/- abdominal distension, harsh lung sounds and crackles, heart murmur and arrhythmia - 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 - 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 - Prognosis is guarded :(
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?
- DCM is a primary myocardial disease characterized by left-sided cardiac enlargement and impaired systolic function.
- 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) - 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 - 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 - 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)
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?
- Arrhythmogenic Right Ventricular Cardiomyopathy
- Autosomal dominant, primarily boxer dogs
- Syncope; Can cause sudden death even in young dogs.
- 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. - 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 - 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.
Topic: Mitral Valve Dysplasia
Topic: Toxocara spp.
- What are the clinical signs associated with this parasite?
- Describe the pathogenesis
- Are they zoonotic?
- 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 - 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.
- High zoonotic potential; T. canis in particular is associated with visceral larval migrans in humans
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?
- dogs
- small intestine
- Transplacental/Transuterine (most common)
- Ingestion of eggs with L3 larvae
- Ingestion of paratenic host
- Transmammary
- fecal flotation
- Fenbendazole, Milbemycin oxime, Moxidectin, Pyrantel
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?
- cats and dogs
- small intestine
- Ingestion of eggs infected with L3 larvae
- Ingestion of paratenic host
- fecal flotation
- Unlike other Toxocara species, migration outside the gastrointestinal tract doesn’t occur
- Fenbendazole, Milbemycin oxime, Moxidectin, Pyrantel
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?
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
What parasite is this?
Toxocara canis from canine.
What parasite is this?
Toxocara cati
What parasite is this?
Toxocara spp. eggs
Looks like a little bowl with some miso soup in it!
Topic: Ancyclostoma spp.
1. What are the clinical signs associated with this parasite?
2. Are they zoonotic?
- 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 - Ancylostoma spp are associated with high zoonotic potential. Associated with cutaneous larval migrans in humans
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?
- dogs
- small intestine
- a. Transmammary (important route)
b. Ingestion of L3 larvae
c. Ingestion of paratenic hosts
d. Transplacental infection
e. Third stage larva penetrate skin - fecal flotation
- For adult A. caninum:
- Fenbendazole
- Milbemycin oxime
- Moxidectin
- Pyrantel pamoate
For L4 A. caninum:
Moxidectin
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?
- dogs and cats
- small intestine
- a. Oral ingestion of 3rd stage larvae
b. Larval penetration of the skin
c. Ingestion of paratenic hosts
d. Transmammary/transplacental - fecal flotation
- For adult A. braziliense in dogs: Pyrantel pamoate
Ancyclostoma spp. is also known as ?
What is important to remember about Ancyclostoma spp. ?
Where are these worms mainly located?
The canine and feline hookworm
Ancylostoma spp are associated with high zoonotic potential. Associated with cutaneous larval migrans in humans
The small intestine