CANINE
Welcome to the Canine Internal Medicine section — your go-to resource for mastering the medical conditions most commonly seen in practice and on the NAVLE.
From gastrointestinal disorders to hepatic, renal, and immune-mediated diseases, this section breaks down complex topics into clear, exam-focused notes. You’ll review pathophysiology, clinical signs, diagnostics, treatment plans, and key decision-making points to help you feel confident when tackling case-based questions. Whether you're reviewing IMHA, or chronic kidney disease, you’ll find everything you need right here to solidify your knowledge and succeed on test day.
Notes:
Disseminated Intravascular Coagulation (DIC) in Dogs & Cats
Disseminated Intravascular Coagulation (DIC) is a critical hemostatic disorder in dogs and cats that occurs exclusively as a complication of an underlying disease process. It is defined by uncontrolled, systemic activation of coagulation pathways leading to widespread microthrombosis, consumption of clotting factors, and ultimately, a paradoxical bleeding tendency. The condition represents a continuum—from subtle, chronic forms with minimal clinical evidence to acute, fulminant presentations characterized by severe hemorrhage and multiorgan dysfunction. Common triggers include sepsis, immune-mediated hemolytic anemia, severe trauma, heat stroke, pancreatitis, and certain neoplasms. Because of its complex pathophysiology, rapid evolution, and poor prognosis, early recognition of clinical signs and interpretation of coagulation profiles are essential for diagnosis and management.
Canine Congenital Portosystemic Shunts (CPSS)
Congenital portosystemic shunts are vascular anomalies that allow portal blood to bypass the liver, leading to hepatic insufficiency and accumulation of toxins such as ammonia. Affected dogs, often small or toy breeds (e.g., Yorkshire Terriers), show signs of hepatic encephalopathy, poor growth, vomiting, and urinary issues due to ammonium biurate uroliths. Diagnosis involves bile acids testing, ammonia levels, and advanced imaging (ultrasound, CT angiography).
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Question 1:
A 6-month-old Yorkshire Terrier presents with intermittent seizures, lethargy, hypersalivation, and stunted growth. The owner reports the signs are worse after meals. CBC shows microcytic, normochromic anemia. Serum bile acids are markedly elevated. What is the most likely diagnosis?
A. Hepatic lipidosis
B. Congenital portosystemic shunt
C. Extrahepatic biliary obstruction
D. Copper storage hepatopathy
Question 2:
A 7-month-old Maltese diagnosed with an extrahepatic congenital portosystemic shunt is undergoing medical stabilization before surgery. Which of the following is the most appropriate medical management strategy before surgical correction?
A. High-fat diet, phenobarbital, vitamin K
B. High-protein diet, prednisolone, lactulose
C. Low-protein diet, lactulose, metronidazole
D. Low-protein diet, omeprazole, cisapride
Answers:
Answer: B) Congenital portosystemic shunt
📘 Explanation:
Congenital portosystemic shunts (CPSS) are vascular anomalies allowing portal blood to bypass hepatic metabolism and flow directly into systemic circulation. They are classified as extrahepatic (most common in small breeds like Yorkies, Maltese, Pugs) or intrahepatic (more common in large breeds like Irish Wolfhounds, Labrador Retrievers).
This condition leads to accumulation of gut-derived toxins, including ammonia, causing hepatic encephalopathy—with neurologic signs worsened after eating due to postprandial ammonia spikes.
Common clinical findings:
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Seizures, disorientation, behavior changes
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Stunted growth, failure to thrive
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GI signs: vomiting, diarrhea, ptyalism
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Urate urolithiasis
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Elevated fasting/postprandial bile acids
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Microcytic anemia, hypoalbuminemia, hypoglycemia
Diagnosis involves:
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Bile acids stimulation test
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Ammonia levels
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Abdominal ultrasound or nuclear scintigraphy to visualize shunt
Question 2:
Answer: C) Low-protein diet, lactulose, metronidazole
📘 Explanation:
Medical management for CPSS is aimed at reducing production and absorption of neurotoxins, especially ammonia, before surgical attenuation of the shunt.
Key strategies:
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Low-protein diet: Decreases ammonia production by gut flora
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Lactulose: Acidifies colonic contents, converting ammonia to non-absorbable ammonium; also acts as a laxative to reduce colonic transit time
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Antibiotics (e.g., metronidazole or neomycin): Reduce urease-producing intestinal bacteria
Other supportive measures:
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Anticonvulsants if seizures are present (avoid benzodiazepines)
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S-adenosylmethionine (SAMe), silymarin for hepatic support
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Surgical options: Ameroid constrictor or cellophane banding to allow gradual occlusion
Prognosis:
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Excellent with successful surgical correction
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Medical management alone improves quality of life but does not eliminate the shunt
