Diagnostic Patterns

• regenerative anemia + inflammatory leukogram,
• spherocytes, agglutination, Heinz bodies, ghost cells, or schistocytes
  
• hyperbilirubinemia (mild to severe)
  
• Hyperlipidemia (cholesterol or triglycerides)
  
• +/- normal ALP and GGT
  

• hyperbilirubinemia (mild to moderate)
  
• Hyperlipidemia (cholesterol or triglycerides)
  
• ALP/GGT +/- increase
  

• increase in ALP/GGT
  
• Hyperlipidemia (cholesterol or triglycerides)
  
• hyperbilirubinemia (mild to severe)
  

• high ALP with NORMAL GGT
  
• increased Heinz bodies
  

• leukocytosis
  
• pre-renal azotemia
  
• increased liver enzymes
  
• post-hepatic cholestasis
  
• hyperglycemia
  
• hypocalcemia
  
• significantly increased amylase
  
• increased lipase
  
• increased TLI

• low albumin, cholesterol, glucose, BUN
  
• prolonged PT and PTT
  
• hyperbilirubinemia (mild to moderate with cholestasis)
  
• increased bile acids, ammonia
  
• decreased USG
• liver enzymes unpredictable

• hyperbilirubinemia (mild to severe)
  
• regenerative anemia (usually)
• spherocytes, agglutination, large numbers of Heinzbodies, RBC ghosts or schistocytes.
  
• Intravascular: hemolyzed plasma
• Extravascular: icteric plasma (may also be from cholestasis)
• Cholestatic enzymes often normal
  

• severe cholestasis causes hepatocellular damage
  
• severe hepatocellular damage can cause cholestasis secondary to cellularswelling and occlusion of the bile ducts,
  
• severe hepatocellular damage canlead to decreased liver function.
  

• severe inflammatory leukogram
  
• hypoglycemia
  
• hepatic cholestasis
  
• thrombocytopenia (moderate)
  
• increased PT, PTT,BMBT, FDPs,
  
• schistocytes/keratocytes
• decreased fibrinogen (least reliable)
• bone marrow necrosis

• microcytic anemia
  
• decreased cholesterol
  
• decreased BUN
  
• increased serum bile acids
  

• albuminmay decrease,
• globulins may increase, then decrease when colostrum is made
  

• Must be severe to result in hypoproteinemia, and albumin is affectedbefore globulins. Effects are reversible.
  
• rarely a cause of hypoglycemia

• Albumin can decrease after serious injury orillness as proteins are required for other purposes
  
• hyperglycemia

• increased fibrinogen
• increased globulins (usually polyclonal)
• decreased albumin

well or overconditioned dairy cows afterparturition, especially with metritis,retained membranes, mastitis, DA or parturient paresis.

Negative energy balance during the peripartum period is associated with mobilization of fat to the liver. Liver enzymes are sometimes but not always elevated, free fatty acids (FFAs) may be increased.

Liver biopsy is usually needed for diagnosis.

Toxemia usually occurs in thelast few weeks of gestation due to negative energy balance associated withrapid fetal growth and insufficient caloric intake.

Usually characterized byketonuria/ketonemia with acidosis (ketones act as acids in the body). FFAlevels are very high.

• hyperglycemia (causes fluid shift into vasculature-hyponatremia and hypochloridemia)
  
• hypercholesterolemia
  
• hepatic lipidosis (increased ALT/AST, heinz bodies, acanthocytes)
  
• increased ALP/ALT
  
• hyperbilirubenemia (post-hepatic cholestasis)
  
• increased Heinz bodies

• poorly concentrated urine (osmotic diuresis/renal azotemia)
  
• acetonuria (likely increased anion gap and/or decreased bicarb)
  
• glucosuria

• hypoglycemia
  
• increased cholesterol
  
• increased ALT (dog)

• steroid leukogram
  
• hyperglycemia
  
• hypercholesterolemia
  
• increased ALP (dog), increased ALT
  
• decreased thyroid,
  
• UA-poorly concentrated urine(corticosteroid-induced resistance to ADH)

• hyperglycemia
  
• increased Heinz bodies
  
• increasedALP (cat)
  
• increased ALT (cat)
  

• pre-renal azotemia
  
• any/all liver enzymes can increase
  
• Increased anion gap
  

• decreased bicarbonate with increased anion gap,
• hypocalcemia (mild) - chelated to form calcium oxlate crystals
  
• hyperphosphatemia - high levels in antifreeze, later due to acute renal failure
  

• hypercalcemia (total and ionized),
  
• +/- hypophosphatemia (classically low, raised to normal with secondary renal failure)
  
• Increased serum PTH
  
• UA: poorly concentrated urine (impaired response to ADH in DCTs)

• Mildhypercalcemiacaused by glucocorticoid deficiency -- protein-bound Ca sosoft-tissue mineralization is unlikely
  
• Hyperphosphatemia (mild) due to hypovolemia (dehydration) and subsequent decreases in GFR
  

• Increasedtotal and ionized Ca
  
• Phosphorus level should be low but possible increase due to secondary renal failure
• PTHrpmay be increased
  
• DecreasedPTH level (due to hypercalcemia)

• Most common cause of hyperphosphatemia (decreased filtration of P)
  
• Calcium concentration is usually normal with prerenal and post-renal azotemia,but can be either normal, increased, or decreased with renal disease
  

• hyperkalemia
  
• increased CK
  
• inflammatory leukogram
  
• hemorrhagic, chylous or suppurative effusions
  
• increased D-dimer

• hypo/hypernatremia- water loss or sodiumloss
  
• low sodium and chloride + high potassium

• low albumin
  
• proteinuria (rule out other sources ofprotein in urinary tract)
  
• +/- increased cholesterol

• decreased TLI
  
• hyperglycemia (due to low insulin)
  

• disproportionate Cl- loss
  
• increased bicarbonate = alkalosis
  
• often dehydration- pre-renal azotemia, hyperalbuminemia, relative polycythemia
  

• low Na, Ca
  
• high K
  
• post-renal azotemia
  
• effusion: low TNCC and TP at first, degenerateneutrophils, effusion has HIGH creatinine (2x serum Creat value)
  

• Heinz bodies
• spherocytes

• basophilic stippling
  
• metarubricytes
  

• increased ammonia
  
• hyperglycemia
  
• increased ALP
  
• can be protein losing enteropathy (lose antithrombin III)
  
• pre-renal azotemia (due to dehydration/hypoperfusion) but can lead to renal if prolonged
  
• Decreased Ca, normal P (unless decreased GFR -> increased P)
  
• Increased CK
  

• regenerativemacrocytic, hypochromic anemia likely
  
• spherocytes
  
• agglutination
  
• positive Coomb’s test
  
• Inflammatory leukogram
  
• hemoglobinemia/uria (if intravascularhemolysis)
  
• icterus (if extravascular hemolysis)
  

• lymphopenia
  
• decreased antithrombin III
  
• panhypoproteinemia
  

• hepatic cholestasis: increased bilirubin, increased ALP/GGT, increasedcholesterol
  
• renal azotemia