Canine Internal Medicine Flashcards

A 7-year-old Golden Retriever presents with polyuria, polydipsia, and a pendulous abdomen. Urinalysis reveals isosthenuria (USG 1.008) and glucosuria with a normal blood glucose of 95 mg/dL. Abdominal ultrasound shows bilateral adrenomegaly. Which mechanism best explains the glucosuria in this patient?

Answer: Renal tubular dysfunction secondary to hypercortisolism causing a Fanconi-like syndrome

Hyperadrenocorticism (Cushing's syndrome) can cause proximal renal tubular dysfunction resembling Fanconi syndrome, leading to glucosuria, aminoaciduria, and phosphaturia despite normoglycemia. The bilateral adrenomegaly, classic clinical signs, and isosthenuria all point to pituitary-dependent hyperadrenocorticism. The glucosuria here is not due to hyperglycemia exceeding the renal threshold but rather impaired tubular reabsorption. Primary renal glucosuria from SGLT2 mutations is rare in dogs, and the clinical picture does not support transient hyperglycemia or stress normalization.

A 4-year-old male intact Labrador Retriever is presented for acute collapse. ECG shows a ventricular rate of 280 bpm with wide, bizarre QRS complexes and no discernible P waves. Blood pressure is 60/40 mmHg. The dog ate a large meal 3 hours ago and the owner notes intermittent exercise intolerance for 2 months. Cardiac troponin I is markedly elevated. What is the MOST likely underlying diagnosis driving this arrhythmia?

Answer: Arrhythmogenic right ventricular cardiomyopathy (ARVC)

Arrhythmogenic right ventricular cardiomyopathy (ARVC) is a heritable cardiomyopathy particularly prevalent in Boxers but also documented in Labrador Retrievers. It is characterized by fibrofatty replacement of right ventricular myocardium and a propensity for sustained ventricular tachycardia and sudden death, often without concurrent structural dilation. The elevated troponin I reflects myocardial injury, the history of exercise intolerance suggests a chronic underlying process, and the arrhythmia morphology is consistent with a right ventricular origin. Dilated cardiomyopathy typically shows systolic dysfunction on echo; GDV arrhythmias are usually less organized; hypokalemia alone rarely causes rates this high with this degree of hemodynamic compromise.

A 9-year-old spayed female Miniature Schnauzer presents with a 3-week history of anorexia, vomiting, and icterus. Serum chemistry reveals: ALT 820 U/L, ALP 2400 U/L, total bilirubin 8.2 mg/dL, cholesterol 620 mg/dL, and triglycerides 1850 mg/dL. Urinalysis shows bilirubinuria and ammonium biurate crystals. Abdominal ultrasound reveals a markedly hyperechoic liver with diffuse loss of portal vein contrast. What is the MOST specific mechanism linking the hyperlipidemia to the liver disease in this patient?

Answer: Reduced hepatic lipoprotein lipase activity and impaired VLDL clearance due to cholestasis

Cholestasis impairs the normal biliary excretion of cholesterol and disrupts the enterohepatic circulation of bile acids. This leads to reduced hepatic lipoprotein lipase activity and impaired clearance of VLDL and chylomicrons, resulting in secondary hyperlipidemia. In this dog, the marked ALP elevation, hypercholesterolemia, and hypertriglyceridemia with icterus are consistent with severe cholestatic liver disease—most likely vacuolar hepatopathy or hepatic lipidosis compounded by the breed's lipid metabolism tendencies. While Miniature Schnauzers have a breed predisposition to primary hypertriglyceridemia, the degree of icterus and transaminase elevation indicates cholestasis is the primary driver of the current lipid abnormalities. The ammonium biurate crystals indicate concurrent portosystemic shunting or severe hepatic failure.

A 6-year-old male neutered Domestic Shorthair cat is evaluated for a 6-month history of weight loss despite polyphagia, intermittent vomiting, and hyperactivity. T4 is 7.8 µg/dL (reference: 0.8–4.0). You initiate methimazole therapy. Four weeks later, the owner reports the cat is less active and has developed facial pruritus and excoriations. Repeat T4 is now 1.2 µg/dL. Creatinine has risen from 1.2 to 3.8 mg/dL. Which pathophysiological explanation BEST accounts for the creatinine increase?

Answer: Unmasking of pre-existing chronic kidney disease as hyperthyroidism-driven hyperfiltration is corrected

Hyperthyroidism increases cardiac output and renal blood flow, creating a state of hyperfiltration that artificially elevates GFR and masks underlying chronic kidney disease (CKD). When hyperthyroidism is treated and T4 normalizes, renal perfusion returns to baseline, revealing the true (and reduced) GFR. This is a well-recognized clinical phenomenon in cats—treating hyperthyroidism can unmask occult CKD, and creatinine rising post-treatment reflects true underlying renal insufficiency, not treatment-induced nephrotoxicity. Methimazole can rarely cause immune-mediated glomerulonephritis, but the facial excoriations here represent a common idiosyncratic skin reaction to methimazole, not nephritis. The timing and magnitude of creatinine rise best fits unmasking rather than dehydration or muscle wasting.

A 5-year-old intact female German Shepherd Dog presents with a 3-week history of protein-losing enteropathy confirmed by a serum albumin of 1.1 g/dL and alpha-1 protease inhibitor fecal test positivity. Endoscopic biopsies reveal lymphangiectasia with marked villous blunting and diffuse mucosal infiltration with CD3+ lymphocytes and plasma cells. Despite 6 weeks of dietary hydrolyzed protein with ultra-low fat and prednisolone (2 mg/kg/day), albumin remains at 1.2 g/dL. What is the MOST appropriate next therapeutic escalation?

Answer: Addition of cyclosporine at 5 mg/kg/day PO as a steroid-sparing immunomodulator

In refractory protein-losing enteropathy (PLE) with immunoproliferative enteropathy in German Shepherd Dogs, failure to respond adequately to dietary management and corticosteroid monotherapy warrants addition of a second immunosuppressive agent. Cyclosporine at 5 mg/kg/day has demonstrated efficacy as a steroid-sparing agent in refractory inflammatory bowel disease and PLE in dogs, reducing corticosteroid requirements and improving clinical outcomes. While cobalamin deficiency is common in chronic enteropathy and should be addressed concurrently, this dog has already been treated for 6 weeks without response, making a watchful waiting approach inappropriate. Switching to a chlorambucil protocol is premature without histologic evidence of clonality (e.g., PARR testing) confirming lymphoma. Total parenteral nutrition is a temporizing measure but does not address the underlying immune-mediated pathology.

A 10-year-old male neutered Cavalier King Charles Spaniel with known myxomatous mitral valve disease (MMVD) stage C1 (compensated heart failure on furosemide, enalapril, and pimobendan) presents for re-evaluation. Recent echocardiography shows LA:Ao of 2.1 and fractional shortening of 18%. The owner reports increased resting respiratory rate of 42 breaths/min over the past week. Thoracic radiographs confirm pulmonary venous congestion without alveolar edema. Serum creatinine is 2.4 mg/dL (up from 1.6 mg/dL at last visit 6 weeks ago). BUN is 58 mg/dL. What is the MOST appropriate immediate management adjustment?

Answer: Increase furosemide dose by 50% and recheck electrolytes and renal values in 5–7 days

This dog is showing early decompensation evidenced by elevated resting respiratory rate and pulmonary venous congestion on radiographs despite current therapy, indicating insufficient diuresis. Increasing furosemide dose by 50% is the appropriate first step to address the fluid overload, with close monitoring of renal values and electrolytes in 5–7 days given the concurrent rise in creatinine—likely due to reduced forward perfusion from poor cardiac output. Discontinuing the ACE inhibitor (enalapril) is contraindicated in heart failure management as it provides vital neurohormonal blockade and is nephroprotective in this setting. Adding spironolactone without increasing the loop diuretic is unlikely to adequately address the active fluid accumulation. Amlodipine is not a first-line agent for MMVD-CHF without concurrent systemic hypertension; it would not address the primary issue of volume overload.