Small Animal Internal Medicine Flashcards

A 7-year-old intact male Shetland Sheepdog presents with PU/PD, bilateral symmetric alopecia, and muscle wasting. Baseline cortisol is 2.1 µg/dL. An ACTH stimulation test yields a post-stimulation cortisol of 24.3 µg/dL. Abdominal ultrasound reveals bilaterally enlarged adrenal glands. Which additional diagnostic finding would most strongly support a diagnosis of pituitary-dependent hyperadrenocorticism over adrenal-dependent disease?

Answer: Suppression of cortisol below 50% of baseline on high-dose dexamethasone suppression test

In pituitary-dependent hyperadrenocorticism (PDH), the pituitary corticotroph tumor retains some negative feedback sensitivity to glucocorticoids. A high-dose dexamethasone suppression test (0.1 mg/kg IV) suppresses cortisol below 50% of baseline in approximately 75–80% of PDH cases, because the pituitary adenoma can still be partially inhibited. Adrenal-dependent tumors are autonomous and will NOT suppress regardless of dexamethasone dose. Bilateral adrenomegaly alone is consistent with PDH (bilateral cortical hyperplasia) but can occasionally be seen with bilateral adrenal tumors. The ACTH stimulation result confirms HAC but does not differentiate origin. UCCR is a sensitive screening tool but lacks specificity for differentiating PDH from ADH.

A 9-year-old spayed female Doberman Pinscher with a known history of dilated cardiomyopathy (DCM) is managed on pimobendan, furosemide, and enalapril. She presents in moderate respiratory distress. Thoracic radiographs confirm severe pulmonary edema. Despite aggressive furosemide therapy (4 mg/kg IV q1h × 2 doses), her respiratory rate remains elevated and her SpO₂ is 88% on room air. Which pharmacological intervention is most appropriate as an adjunct at this stage?

Answer: Administer nitroprusside IV infusion to reduce ventricular afterload

In refractory cardiogenic pulmonary edema unresponsive to loop diuretics, IV nitroprusside (a balanced arterial and venous vasodilator) reduces both preload and afterload, acutely lowering filling pressures and improving forward flow. This is particularly useful in DCM where high systemic vascular resistance worsens pump failure. Dobutamine is reserved for cardiogenic shock with low output/hypotension; this patient's presentation prioritizes afterload reduction over inotropy. Digoxin has a narrow therapeutic index, slow onset, and limited acute utility in this context. Spironolactone acts too slowly (days to weeks) to benefit an acute crisis.

A 5-year-old castrated male Domestic Shorthair cat presents with a 3-week history of weight loss, increased appetite, and intermittent vomiting. Total T4 is 2.8 µg/dL (reference: 0.8–4.0 µg/dL), which is within normal limits. However, clinical suspicion for hyperthyroidism remains high based on physical examination findings. Which next step is most diagnostically appropriate?

Answer: Measure free T4 by equilibrium dialysis (fT4 ED)

Approximately 10% of hyperthyroid cats have a normal total T4 due to concurrent non-thyroidal illness (euthyroid sick syndrome) suppressing T4 into the reference range — a phenomenon called 'masking.' Free T4 measured by equilibrium dialysis (fT4 ED) is not affected by binding protein changes and is elevated in most of these cases, making it the most sensitive next step when total T4 is equivocal in a cat with strong clinical signs. The T3 suppression test is used in early/mild cases but is logistically cumbersome. A methimazole trial without confirmation can mask concurrent disease. Repeating total T4 is reasonable but fT4 ED provides earlier and more reliable discrimination.

A 6-year-old intact female Golden Retriever presents with a 10-day history of polydipsia, purulent vaginal discharge, and lethargy. Abdominal ultrasound confirms a distended uterus. CBC reveals a WBC of 38,000 cells/µL with a left shift. Blood chemistry shows BUN 48 mg/dL, creatinine 2.1 mg/dL, and phosphorus 6.8 mg/dL. After initial IV fluid stabilization, the patient is scheduled for ovariohysterectomy. In the perioperative period, which renal pathophysiology finding is most specifically associated with pyometra-induced nephropathy in dogs?

Answer: Immune-complex glomerulonephritis with IgG and complement deposition in glomerular capillaries

Pyometra-associated nephropathy in dogs is characteristically caused by immune-complex deposition in glomeruli. The chronic bacterial infection (usually E. coli) drives sustained antigenemia, leading to circulating antigen-antibody complexes that deposit in the glomerular basement membrane, activating complement and causing membranoproliferative-type glomerulonephritis. This can result in proteinuria, azotemia, and even permanent CKD if untreated. Renal medullary washout (choice C) does contribute to the PU/PD and decreased urine specific gravity, but this is a functional and reversible change, not the defining pathological lesion. Tubular necrosis and obstructive pyelonephritis are less characteristically associated with the specific renal lesion of pyometra.

A 4-year-old Labrador Retriever presents with acute collapse, severe abdominal pain, and pale mucous membranes. On auscultation, heart sounds are muffled. Jugular venous distension is present. ECG shows sinus tachycardia with low-amplitude complexes and electrical alternans. FAST ultrasound reveals a large pericardial effusion. After emergency pericardiocentesis, 400 mL of serosanguineous fluid is drained and the dog stabilizes. Cytology of the fluid shows a mixed inflammatory population with no detectable neoplastic cells. Which statement about this patient's prognosis and management is most accurate?

Answer: Idiopathic pericardial effusion has a high recurrence rate, and pericardiectomy should be offered after two or more recurrences

Pericardial effusion in large-breed dogs is most commonly caused by cardiac neoplasia (hemangiosarcoma, chemodectoma) or idiopathic pericarditis. Critically, cytology of pericardial fluid has poor sensitivity for detecting neoplastic cells — particularly with hemangiosarcoma, which exfoliates poorly — so a negative cytology does NOT exclude neoplasia (making choice A incorrect). For confirmed or suspected idiopathic pericardial effusion, management involves pericardiocentesis for acute relief. Recurrence is common (up to 50%), and pericardiectomy (subtotal or total) is the preferred long-term treatment after two or more recurrences, offering excellent outcomes for idiopathic disease. Corticosteroids are not routinely recommended immediately post-drainage without a confirmed inflammatory etiology. Labradors, not Golden Retrievers, are the breed in this question; Golden Retrievers have a high association with HSA and chemodectoma.

A 10-year-old spayed female Miniature Schnauzer presents with acute pancreatitis confirmed by elevated cPLI, abdominal pain, and characteristic ultrasonographic findings. On day 3 of hospitalization, she develops progressive icterus. Bilirubin is 8.4 mg/dL (predominantly direct). ALP is 1,240 U/L; ALT is 680 U/L. Abdominal ultrasound now shows marked dilation of the common bile duct. Which is the most likely cause of the extrahepatic biliary obstruction in this case, and what is the appropriate next management step?

Answer: Inspissated bile or fibrotic stricture from periductal inflammation; surgical biliary diversion should be pursued urgently if obstruction persists beyond 5–7 days

Extrahepatic biliary obstruction (EHBO) is a recognized complication of severe pancreatitis in dogs, resulting from periductal edema, adhesions, inspissated bile, or fibrotic stricture from ongoing inflammation around the common bile duct. The markedly elevated direct bilirubin and dilated common bile duct on ultrasound confirm post-hepatic (obstructive) cause. Initial management includes medical stabilization, nutritional support, and close monitoring. If obstruction does not resolve within 5–7 days — or worsens — surgical biliary diversion (e.g., cholecystoduodenostomy or choledochoduodenostomy) is required to prevent progressive hepatic damage and biliary sepsis. Gallbladder mucocele rupture would present with bile peritonitis signs (sepsis, peritoneal free fluid with bile staining) and requires more urgent surgery. Hepatic lipidosis causes intrahepatic cholestasis, not bile duct dilation. Ascending cholangitis alone doesn't explain the mechanical ductal dilation.