Large Animal Internal Medicine Flashcards

A 6-year-old Quarter Horse mare presents with acute onset of severe colic, tachycardia (72 bpm), and markedly elevated peritoneal fluid total protein (4.8 g/dL) with a nucleated cell count of 95,000 cells/µL. Nasogastric reflux yields 8 liters of fluid. Rectal palpation reveals a taut, gas-distended viscus in the left dorsal quadrant that cannot be decompressed. Which diagnosis best fits this presentation?

Answer: Left dorsal displacement of the large colon with concurrent small intestinal strangulation

The combination of markedly abnormal peritoneal fluid (elevated protein and very high nucleated cell count) indicating devitalized bowel, large-volume nasogastric reflux indicating small intestinal involvement, and a non-reducible gas-distended viscus in the left dorsal quadrant points to a combined lesion — left dorsal displacement of the large colon concurrent with a small intestinal strangulating obstruction. Nephrosplenic entrapment alone would not produce peritoneal fluid changes of this severity, nor would it typically cause substantial nasogastric reflux. Large colon volvulus could explain the abnormal peritoneal fluid but typically does not produce high-volume reflux. Duodenojejunal obstruction would not place a distended viscus in the left dorsal quadrant.

A 4-year-old Thoroughbred gelding is evaluated for intermittent exercise intolerance and post-exertional muscle stiffness. Serum CK peaks at 48,000 IU/L four hours after moderate exercise. A muscle biopsy reveals abnormal polysaccharide inclusions that stain positively with PAS but are resistant to diastase digestion. Genetic testing is NEGATIVE for the GYS1 mutation. Which condition is most likely responsible?

Answer: Polysaccharide storage myopathy type 2 (PSSM2)

PSSM type 1 is caused by a gain-of-function mutation in the GYS1 gene (glycogen synthase) and produces diastase-resistant PAS-positive inclusions. However, since GYS1 testing is negative, PSSM type 2 is the correct diagnosis. PSSM2 has similar histopathological findings (diastase-resistant PAS-positive inclusions) but is not caused by the GYS1 mutation; its genetic basis involves other variants (e.g., MYH1 mutations in some cases). RER typically does not produce abnormal polysaccharide inclusions on biopsy. Malignant hyperthermia is triggered by volatile anesthetics and is not associated with polysaccharide storage on biopsy.

A 10-year-old Holstein cow in late gestation is found recumbent and unable to rise. Physical examination reveals decreased mentation, a distended abdomen, and hypocalcemia confirmed on blood chemistry. Despite two treatments with IV calcium borogluconate (500 mL of 23% solution each), the cow remains recumbent. Serum magnesium is 0.4 mEq/L (reference: 1.8–2.3 mEq/L). Which pathophysiologic mechanism best explains the refractory hypocalcemia in this case?

Answer: Hypomagnesemia impairs both parathyroid hormone secretion and end-organ responsiveness to PTH

Magnesium is essential for both the secretion of parathyroid hormone (PTH) from the parathyroid gland and the responsiveness of target tissues (bone, kidney) to PTH. Severe hypomagnesemia (as seen here) causes functional hypoparathyroidism, making calcium supplementation ineffective until magnesium is corrected. This is a well-recognized cause of refractory milk fever in cattle. While hypophosphatemia can accompany hypocalcemia, it does not directly impair response to IV calcium. Calcitonin receptor downregulation does not occur with therapeutic calcium doses. Hepatic 25-hydroxylation impairment (fatty liver) is a recognized risk factor for hypocalcemia but would not fully explain the acute refractory response to IV calcium given the profound hypomagnesemia.

A 3-week-old foal presents with bilateral uveitis, polyarthritis, hypopyon, and a serum IgG of 200 mg/dL. Blood culture is pending. Which pathogen, if isolated, would MOST strongly support a diagnosis of Rhodococcus equi?

Answer: A gram-positive, weakly acid-fast, pleomorphic coccobacillus that is catalase and urease positive

Rhodococcus equi is a gram-positive, pleomorphic coccobacillus that is weakly acid-fast (Ziehl-Neelsen positive), catalase positive, and urease positive. It is the classic cause of suppurative pneumonia in foals 1–6 months old and can cause extrapulmonary lesions including uveitis, polyarthritis, and hypopyon, particularly in immunocompromised foals (failure of passive transfer with IgG of 200 mg/dL is severe FPT). The other choices describe organisms inconsistent with R. equi: gram-negative encapsulated rods suggest Klebsiella or Mannheimia; beta-hemolytic gram-positive chains suggest Streptococcus; lactose-fermenting gram-negative motile rods suggest Enterobacteriaceae such as E. coli.

A 7-year-old Angus cow presents with a 3-week history of progressive weight loss, tenesmus, and intermittent blood-tinged feces. Rectal examination reveals a firm, irregular intraluminal mass approximately 15 cm cranial to the anus. Biopsy histopathology shows nests of cells with squamous differentiation and keratin pearls invading the submucosa. Serum calcium is 14.2 mg/dL (reference: 8.4–10.2 mg/dL). Which mechanism most likely accounts for the hypercalcemia?

Answer: Tumor secretion of parathyroid hormone-related protein (PTHrP)

The histopathology describes squamous cell carcinoma (SCC) of the rectum. Humoral hypercalcemia of malignancy (HHM) is the most common cause of paraneoplastic hypercalcemia in large animals, and it is mediated by PTHrP secreted by the tumor. PTHrP mimics PTH at the PTH receptor, causing increased bone resorption, increased renal calcium reabsorption, and decreased renal phosphorus reabsorption. Osteolytic metastases (local osteolysis) are less common in cattle and would be unlikely to cause hypercalcemia of this degree from a rectal primary. Ectopic 1,25-dihydroxyvitamin D production occurs with lymphoma in some species but is not the typical mechanism with SCC. Concurrent primary hyperparathyroidism would be a highly unlikely coincidence.

A 5-year-old llama presents with a 2-month history of progressive weight loss, intermittent regurgitation of third-compartment (C3) contents, and ventral edema. Fecal flotation reveals a high burden of Haemonchus contortus. Serum albumin is 1.1 g/dL (reference: 3.0–4.5 g/dL). A fecal egg count reduction test (FECRT) is performed: pre-treatment count is 4,200 EPG; post-treatment count at 14 days following ivermectin is 3,900 EPG. Which conclusion and next management step are MOST appropriate?

Answer: Ivermectin resistance is confirmed; switch to monepantel or derquantel-abamectin combination and implement targeted selective treatment with FAMACHA scoring

A fecal egg count reduction of less than 95% following anthelmintic treatment is the standard threshold for diagnosing anthelmintic resistance in small ruminants and camelids. Here, the reduction is only ~7% (from 4,200 to 3,900 EPG), which unambiguously confirms high-level ivermectin resistance. The appropriate next step is switching to an anthelmintic class with a different mechanism of action — monepantel (amino-acetonitrile derivative) or derquantel-abamectin combination (spiro-indole). Simply doubling the ivermectin dose is inappropriate and will not overcome high-level receptor-mediated resistance. While immunosuppression can affect worm burdens, a 7% reduction is not attributable to host factors. Larval development assays are confirmatory tools but unnecessary when FECRT already demonstrates clear resistance; delaying treatment change in a hypoalbuminemic animal is clinically dangerous.