Small Animal Internal Medicine Flashcards

A 7-year-old intact male Shar-Pei presents with recurrent fever episodes, swollen hocks, and progressive proteinuria. Renal biopsy reveals amyloid deposits in the medullary interstitium rather than the glomeruli. Which statement best describes the pathophysiology of this condition?

Answer: Shar-Peis uniquely deposit AA amyloid preferentially in the medullary interstitium, causing tubular dysfunction before glomerular disease, and elevated serum amyloid A is driven by chronic IL-6 overproduction due to a hyaluronan metabolism defect.

Shar-Pei fever syndrome is caused by elevated hyaluronan due to a defect in hyaluronidase activity, triggering chronic IL-6 release and sustained serum amyloid A (SAA) elevation. Unlike most breeds where AA amyloidosis deposits in glomeruli, Shar-Peis characteristically deposit amyloid in the medullary interstitium, causing tubular disease and renal papillary necrosis rather than a classic nephrotic presentation early in the course.

A 10-year-old spayed female Doberman Pinscher with dilated cardiomyopathy and recent syncope is being treated with pimobendan, furosemide, and enalapril. An 18-lead Holter monitor reveals 4,800 ventricular premature complexes over 24 hours, including several R-on-T events. The owner reports the dog ate a large meal of canned salmon the previous evening. Which intervention is most appropriate at this point?

Answer: Add mexiletine at 5–8 mg/kg PO TID as the primary antiarrhythmic of choice for Doberman DCM-associated ventricular arrhythmias, and recheck Holter in 4–6 weeks.

Mexiletine is the preferred first-line antiarrhythmic for ventricular arrhythmias in Doberman Pinschers with DCM; it is a Class IB sodium channel blocker well-tolerated in myopathic dogs. Sotalol is a reasonable second choice but carries more negative inotropy risk in decompensated DCM. Pimobendan remains indicated and is not contraindicated by VPC count thresholds. Furosemide-induced hypomagnesemia can contribute but is not the sole driver, and discontinuing it in a volume-overloaded patient would be dangerous. Taurine/carnitine testing is valuable but does not change the immediate antiarrhythmic decision.

A 6-year-old male neutered Golden Retriever presents with polydipsia, polyuria, and a serum calcium of 14.8 mg/dL. PTH is suppressed (<10 pg/mL), PTHrP is undetectable, ionized calcium is elevated, and 1,25-dihydroxyvitamin D (calcitriol) is markedly elevated at three times the upper reference limit. Thoracic and abdominal imaging reveals no obvious masses. Which diagnosis is most consistent with these findings?

Answer: Granulomatous disease (e.g., systemic fungal infection or sterile granuloma) causing PTH-independent, calcitriol-mediated hypercalcemia.

The combination of suppressed PTH, undetectable PTHrP, and markedly elevated 1,25-dihydroxyvitamin D points to ectopic calcitriol production. Granulomatous lesions (macrophages in fungal infections such as blastomycosis, histoplasmosis, or sterile granulomatous disease) contain 1α-hydroxylase activity independent of PTH regulation, producing excess calcitriol and driving intestinal calcium absorption and hypercalcemia. In PTHrP-mediated HHM, calcitriol is typically suppressed or normal, not elevated. Primary HPT suppresses PTHrP and elevates PTH, not suppresses it.

A 9-year-old spayed female DSH cat presents with acute onset of right-sided Horner's syndrome, ipsilateral loss of the palpebral reflex with retained menace, and right thoracic limb monoparesis. An ACTH stimulation test is normal. Thoracic radiographs reveal a cranial mediastinal mass. Which single additional diagnostic finding would most strongly confirm the unifying diagnosis?

Answer: A positive acetylcholine receptor antibody titer confirming paraneoplastic myasthenia gravis, explaining limb weakness while the mass represents a thymic epithelial tumor.

This cat's neurological picture — Horner's syndrome, loss of palpebral reflex with intact menace (suggesting a peripheral CN VII lesion rather than cortical), and limb monoparesis — alongside a cranial mediastinal mass is classic for thymoma with paraneoplastic polyneuropathy and myasthenia gravis. A positive AChR antibody titer would confirm acquired myasthenia gravis (the limb weakness), and thymoma in cats is strongly associated with this paraneoplastic syndrome. Large granular lymphoma does not typically produce these localized cranial nerve and peripheral nerve findings. MRI with spinal extension is a less parsimonious explanation when paraneoplastic disease accounts for all findings.

A 4-year-old male intact Bernese Mountain Dog presents with progressive ascites, hepatomegaly, and elevated liver enzymes. Abdominal ultrasound reveals a severely distended caudal vena cava and hepatic veins with absent pulsatility on Doppler, and a markedly thickened hepatic vein ostium. Portosystemic shunting is absent. Protein-losing nephropathy and protein-losing enteropathy have been ruled out. Which diagnostic test should be prioritized next?

Answer: Right heart catheterization or cardiac CT angiography to evaluate for constrictive pericarditis or Budd-Chiari-like syndrome from hepatic vein or caval obstruction.

The clinical presentation — ascites, hepatomegaly, distended caudal vena cava with hepatic venous outflow obstruction and absent pulsatility on Doppler — is characteristic of Budd-Chiari syndrome or post-hepatic (post-sinusoidal) portal hypertension. In dogs, this can result from right-sided heart failure, constrictive pericarditis, caval thrombosis, or extrinsic compression. Right heart catheterization or cardiac CT angiography is the priority to distinguish cardiac causes (e.g., constrictive pericarditis, which is surgically correctable) from primary vascular obstruction. Liver biopsy before excluding post-hepatic causes risks bleeding and misses the diagnosis; sinusoidal obstruction syndrome does not produce dilated hepatic veins on Doppler.

A 5-year-old female spayed Labrador Retriever is referred for refractory inflammatory bowel disease. She has been on prednisolone 2 mg/kg/day for 8 weeks with minimal response. Endoscopic biopsies show diffuse mucosal eosinophilic infiltration with fibrosis extending into the submucosa, and tissue culture grows Pythium insidiosum. Serology for Pythium-specific ELISA is strongly positive. Which treatment approach is best supported by current evidence?

Answer: Add itraconazole 5 mg/kg PO BID combined with terbinafine 5–10 mg/kg PO daily, as this azole-allylamine combination has the best documented clinical response rate for gastrointestinal pythiosis in dogs, alongside surgical resection of affected bowel if focal.

Pythium insidiosum is an oomycete (water mold), not a true fungus — its cell membrane contains cellulose and non-ergosterol sterols, making it intrinsically resistant to amphotericin B and most azoles. However, the combination of itraconazole and terbinafine has shown the best clinical outcomes in canine gastrointestinal pythiosis by targeting multiple steps in sterol synthesis pathways. Surgical resection of focal lesions combined with medical therapy improves survival. Voriconazole has poor activity against Pythium despite good azole spectrum otherwise. Immunotherapy (Pythium vaccine) exists but is not established as first-line monotherapy and is used as an adjunct.