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Clinical Pathology Case
BY: ABIGAIL SCHMIDT
Signalment: 2 yr 8 mos M Cairn Terrier
History: 6 wks PU/PD;
Drinking 150-300 mls/kg/day
PU/PD Differentials
• Diabetes Mellitus
• Hyperadrenocorticism (Cushing’s)
• Hypoadrenocorticism (Addison’s)
• Renal Disease (CRF)
• Liver Disease
• Neoplasia
– lymphoma, anac sac adenocarcinoma, multiple myeloma,
pheochromocytoma
• Hypercalcemia
• Iatrogenic
– Administration of steroids, diuretics, etc.
• Psychogenic Polydipsia
• The list continues…..
Diagnostics I would pursue
• Urinalysis
• Haematology
• Full Biochemistry
Diagnostics Actually Run…
• Urinalysis (cystocentesis)
– Mild haematuria, otherwise normal
– USG 1.010: Isosthenuric
• Haematology
– Mild leukocytosis and mild neutrophilia  likely a stress
response/mild inflammation
• Biochemistry…
• ACTH Stimulation Test: normal
Normals
Biochemistry
Sodium
Potassium
Na:K ratio
Chloride
Creatinine
Cholesterol
Triglyceride
Total Bilirubin
ALKP
GGT
Albumin:Globulin Ratio
Abnormals
Biochemistry All results mildly…
Calcium 
Phosphate 
Urea 
AST 
ALT 
Total Protein 
Albumin 
Globulin 
Interpretation of Abnormals
• Hypocalcemia  possibly decreased due to low albumin?
• Hyperphosphatemia
• Hypouremia  increased loss (PU)/decreased production
**BUN, albumin, glucose, and cholesterol = often first parameters
decreased with liver function
• Elevated Liver enzymes: AST, ALT
– AST: can be elevated with muscle inflammation or necrosis (e.g. IM muscle
injection, exercise), red blood cell hemolysis, or with liver disease.
– ALT: MOST liver specific enzyme; indicated hepatocellular damage
• Hypoproteinemia
– Hypoalbuminemia
– Hypoglobulinemia
Test Liver for
dysfunction R/O
Protein loss or
malfunction in
protein production
PU/PD Ddx Rule Outs
• Diabetes Mellitus
• Hyperadrenocorticism (Cushing’s)
• Hypoadrenocorticism (Addison’s)
• Renal Disease (CRF)  much less likely
• Liver Disease ***
• Neoplasia
– lymphoma, anac sac adenocarcinoma, multiple myeloma,
pheochromocytoma
• Hypercalcemia
• Iatrogenic
– Administration of steroids, diuretics, etc.
• Psychogenic Polydipsia
Further Tests to Run?
• BILE ACIDS STIMULATION TEST
– Values mild to moderately elevated pre
– Values severely elevated post
– Values even further elevated 2 hrs post
• WORKING DIAGNOSIS…based on signalment, history, urinalysis,
bloods thus far: Liver Disease due to Portosystemic Shunt
– Most likely extrahepatic due to breed (small dog and predisposition of
Cairn Terriers)
– Shunts allow portal blood to reach the systemic circulation w/o first
passing through the liver. Normally blood exiting the intestines, spleen,
and pancreas enters the portal vein, which then takes blood to the liver.
The liver metabolizes and detoxifies this blood. If a shunt is present the
liver is deprived of factors that allow it to fully develop (hepatic
atrophy).
– Hepatic atrophy commonly results in hepatic insufficiency.
Liver Shunt Workup & Treatment
• Ultrasound  microhepatica
• Nuclear scintigraphy  non-invasive colonic
administration of a radioisotope, and measurement of
blood flow
– Computer measures amount of radioactive blood in the
heart and the liver and compares the two
• Portography  radiograph highlighting portal system
after injection of radio-opaque contrast material
• CT Angiography (3D image; assess hepatic vasculature)
• Extrahepatic Shunt: Surgery to
correct; amyloid constrictor bands
Medical Management of Shunt Cases
• Congenital vs. Acquired
• Extrahepatic vs. Intrahepatic
• IV fluids
• Enema to remove intestinal toxins before they can be
absorbed
• DIET: low protein
• Lactulose  alters pH in LI to decrease ammonia and
other toxin absorption; also makes environment
unfavorable to bacteria
• ABs: to reduce number of toxin-producing bacteria in
intestines; also helpful if patient also has a UTI

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PHP Clinical Pathology Case

  • 1. Clinical Pathology Case BY: ABIGAIL SCHMIDT Signalment: 2 yr 8 mos M Cairn Terrier History: 6 wks PU/PD; Drinking 150-300 mls/kg/day
  • 2. PU/PD Differentials • Diabetes Mellitus • Hyperadrenocorticism (Cushing’s) • Hypoadrenocorticism (Addison’s) • Renal Disease (CRF) • Liver Disease • Neoplasia – lymphoma, anac sac adenocarcinoma, multiple myeloma, pheochromocytoma • Hypercalcemia • Iatrogenic – Administration of steroids, diuretics, etc. • Psychogenic Polydipsia • The list continues…..
  • 3. Diagnostics I would pursue • Urinalysis • Haematology • Full Biochemistry
  • 4. Diagnostics Actually Run… • Urinalysis (cystocentesis) – Mild haematuria, otherwise normal – USG 1.010: Isosthenuric • Haematology – Mild leukocytosis and mild neutrophilia  likely a stress response/mild inflammation • Biochemistry… • ACTH Stimulation Test: normal
  • 6. Abnormals Biochemistry All results mildly… Calcium  Phosphate  Urea  AST  ALT  Total Protein  Albumin  Globulin 
  • 7. Interpretation of Abnormals • Hypocalcemia  possibly decreased due to low albumin? • Hyperphosphatemia • Hypouremia  increased loss (PU)/decreased production **BUN, albumin, glucose, and cholesterol = often first parameters decreased with liver function • Elevated Liver enzymes: AST, ALT – AST: can be elevated with muscle inflammation or necrosis (e.g. IM muscle injection, exercise), red blood cell hemolysis, or with liver disease. – ALT: MOST liver specific enzyme; indicated hepatocellular damage • Hypoproteinemia – Hypoalbuminemia – Hypoglobulinemia Test Liver for dysfunction R/O Protein loss or malfunction in protein production
  • 8. PU/PD Ddx Rule Outs • Diabetes Mellitus • Hyperadrenocorticism (Cushing’s) • Hypoadrenocorticism (Addison’s) • Renal Disease (CRF)  much less likely • Liver Disease *** • Neoplasia – lymphoma, anac sac adenocarcinoma, multiple myeloma, pheochromocytoma • Hypercalcemia • Iatrogenic – Administration of steroids, diuretics, etc. • Psychogenic Polydipsia
  • 9. Further Tests to Run? • BILE ACIDS STIMULATION TEST – Values mild to moderately elevated pre – Values severely elevated post – Values even further elevated 2 hrs post • WORKING DIAGNOSIS…based on signalment, history, urinalysis, bloods thus far: Liver Disease due to Portosystemic Shunt – Most likely extrahepatic due to breed (small dog and predisposition of Cairn Terriers) – Shunts allow portal blood to reach the systemic circulation w/o first passing through the liver. Normally blood exiting the intestines, spleen, and pancreas enters the portal vein, which then takes blood to the liver. The liver metabolizes and detoxifies this blood. If a shunt is present the liver is deprived of factors that allow it to fully develop (hepatic atrophy). – Hepatic atrophy commonly results in hepatic insufficiency.
  • 10. Liver Shunt Workup & Treatment • Ultrasound  microhepatica • Nuclear scintigraphy  non-invasive colonic administration of a radioisotope, and measurement of blood flow – Computer measures amount of radioactive blood in the heart and the liver and compares the two • Portography  radiograph highlighting portal system after injection of radio-opaque contrast material • CT Angiography (3D image; assess hepatic vasculature) • Extrahepatic Shunt: Surgery to correct; amyloid constrictor bands
  • 11. Medical Management of Shunt Cases • Congenital vs. Acquired • Extrahepatic vs. Intrahepatic • IV fluids • Enema to remove intestinal toxins before they can be absorbed • DIET: low protein • Lactulose  alters pH in LI to decrease ammonia and other toxin absorption; also makes environment unfavorable to bacteria • ABs: to reduce number of toxin-producing bacteria in intestines; also helpful if patient also has a UTI