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CBC/CHEMISTRY PANEL/URINALYSIS

CBC

WBC

12.6

K/uL

4.5-17.0

RBC

9.69

M/uL

5.00-10.00

HGB

11.9

g/dl

8.0-15.0

HCT

39.3

%

24.0-45.0

MCV

41

fL

39-55

MCH

12.3

pg

12.0-18.0

MCHC

30.3

%

30.0-36.0

Platelet Count

DNR

K/uL

300-800

 

 

 

 

 

ABS

%

 

Baso

0

0

 

Eos

1008

8

 

Bands

0

0

 

Polys

7308

58

 

Lymph

4032

32

 

Monos

252

2

 

 

 

 

 

 

 

 

 

 

 

Slide Review: Platelets clumped. Platelet estimate adequate. RBC morphology normal. No hemobartonella seen.

Chemistry Panel

Glucose, Serum

88

mg/dl

70-125

BUN

16

mg/dl

10-35

Creatinine

1.0

mg/dl

1.0-2.0

Sodium

151

meq/l

145-160

Potassium

4.7

meq/l

4.0-5.8

Sodium/Potassium Ratio

32

 

 

Chloride

118

meq/l

109-128

Carbon Dioxide

19

meq/l

17-24

Anion Gap

14

 

13-25

Calcium

6.8

mg/dl

8.0-12.0

Phosphorus

5.4

mg/dl

3.5-6.1

Osmolality, Calculated

300

 

270-310

Total Protein

6.2

g/dl

3.5-6.1

Albumin

3.3

g/dl

2.6-4.0

Globulin

2.9

g/dl

2.6-5.1

Albumin/Globulin Ratio

1.1

 

0.5-2.0

Bilirubin, Total

0.2

mg/dl

0.0-0.5

Alkaline Phosphatase

397

U/L

10-70

Gamma gt

0

U/L

1-8

ALT

66

U/L

5-65

AST

49

U/L

26-43

Cholesterol

129

mg/dl

75-175

Hemolytic Index

13

mg/dl

 

Lipemic Index

28

mg/dl

 

Icteric Index

0

mg/dl

 

T4, Feline

2.9

ug/dl

1.8-4.5

Urinalysis:

pH

6.0

6.0-9.5

Sp. Gravity

1.039

1.005-1.055

Appearance

Clear

 

Color

Yellow

 

Protein

Neg

 

Glucose

Neg

 

Ketone

Neg

 

Bilirubin

Neg

 

Blood

Neg

 

MICROSCOPIC

 

 

WBC

0

 

RBC

0-4

 

Epith

0

 

Hyal Cast

Neg

 

Gran Cast

Neg

 

RBC Cast

Neg

 

Bacteria

Neg

 

Mucus

Neg

 

Crystals

Neg

 

PROBLEM LIST FROM BLOOD PANEL

·  Hypocalcemia

·  Alkaline Phosphatase Elevation

·  Low Gamma gt

·  ALT Elevation

·  AST Elevation

Hypocalcemia Rule outs:

·  Primary hypoparathyroidism

·  Acute and Chronic Renal Failure

·  Ethylene Glycol Toxicity

·  Acute pancreatitis

·  Intestinal Malabsorption Syndromes

·  Hypoproteinemia or hypoalbuminemia

·  Nutritional Secondary hyperparathyroidism

·  Phosphate – containing enemas

Alkaline Phosphatase Elevation:

Increased serum alkaline phosphatase (SAP) is interpreted differently in dogs and cats. Cats have less hepatocellular SAP, which is readily excreted by their kidneys. Therefore, any increase in feline SAP is considered significant.

·  Young animal

·  Drugs that cause cholestasis or induce hepatic enzymes

·  Bone disease

·  Biliary Tract Abnormalities

·  Cholangiohepatitis

·  Hepatic lipidosis

·  Hepatic lymphoma

·  Feline Infectious Peritonitis

·  Hyperthyroidism

·  Diabetes mellitus

Low Gamma gt

In cats, gamma gt (GGT) has slightly greater sensitivity and perhaps greater specificity for hepatic disease (except hepatic lipidosis) than SAP. GGT is less influenced than SAP by secondary hepatic disease conditions or enzyme-inducing drugs.

Decreased GGT is not significant.

Alanine Transferase (ALT) Elevation

ALT is present in hepatocyte cytosol. Increased ALT reflects cell membrane damage and leakage.

·  Any drug causing hepatocellular damage.

·  Cholangitis/Cholangiohepatitis

·  Feline Infectious Peritonitis

·  Hepatic lymphoma

·  Cirrhosis

·  Trauma

·  Pancreatitis

·  Hyperthyroidism

·  Anoxia from anemia/shock/hemolysis

·  Iatrogenic

Aspartate Transferase Elevation

AST is present in hepatocyte mitochondria. Significant AST elevations tend to reflect more serous hepatic damage because the mitochondria are not damaged as readily as is the cell membrane. However, AST is also present in significant quantities in many other tissues, including muscle and RBC’s.

·  Hepatic disease

·  Muscle inflammation or necrosis

·  Hemolysis – spontaneous or artifactual

Ruleouts

Primary ruleouts from blood panel and radiographs.

1.        Metabolic bone disease

2.        Nutritional secondary hyperparathyroidism

3.       Primary hypoparathyroidism

Metabolic Bone Disease

Metabolic Bone Disease can be used broadly to encompass various conditions that lead to osteopenia. These conditions may include metabolic, nutritional and endocrine bone disorders.

This broad diagnosis is supported by radiographs and blood panel. Further diagnostic tests are warranted to narrow the cause. These include Magnesium, ionized Calcium, and Parathyroid Hormone Levels. Until recently, Calcitriol (1, 25 dihydrocholecalciferol) plasma levels could also be run, however, labs offering this test have discontinued it except on research cases.

Nutritional Secondary Hyperparathyroidism

Nutritional Secondary Hyperparathyroidism is a metabolic disorder in which bone production is normal, but osteopenia results from excessive bone resorption. It is caused by diets providing excess phosphate, insufficient calcium, or both. Affected animals have usually been fed mainly meat, organ tissue, or both.

The clinical history of a "normal kitten diet" does not support this diagnosis.

Primary Hypoparathyroidism

Loss of parathyroid function leads to decreased serum calcium and increased serum phosphate. These changes are due to loss of Parathyroid Hormone (PTH) effects on mobilization of calcium and phosphate from bone, renal retention of calcium, enhanced renal excretion of phosphate, and increased absorption of calcium and phosphate from intestine.

This diagnosis occurs more commonly in cats having undergone thyroidectomy and inadvertent parathyroidectomy. It rarely occurs naturally, and in those situations, the clinical course includes neurologic or neuromuscular disturbances. This diagnosis is unlikely in this kitten since there are no clinical signs of neurologic or neuromuscular disease.

Ionized Calcium (iCa)

iCalcium = 0.9 (1.25-1.45 mmol/L)

Parathyroid Hormone (PTH)

PTH = 24.2 (2-13 pmol/L)

Magnesium

Mg = 2.2 mg/dl (2.0-2.5 mg/dl)

Interpretation of PTH, Mg and iCa Results:

The magnesium level is normal. Hypomagnesemia can cause hypocalcemia. Severe hypomagnesemia in humans can cause inhibition of PTH secretion or synthesis.

An elevated PTH level rules out primary hypoparathyroidism. An elevated PTH in the presence of a low iCa confirms a Vitamin D anomaly. There are three types of Vitamin D anomalies, including Vitamin D deficiency and Type I and Type II Vitamin D-dependent rickets. Unfortunately, to further differentiate these diseases prior to treatment, a plasma Calcitriol level would be needed. Since this test is not available currently, response to therapy is the only way to attempt to differentiate these Vitamin D anomalies.

Vitamin D deficiency includes defects in absorption of Vitamin D from the gastrointestinal tract. Type I rickets is attributable to a defect in Calcitriol production by the renal 1α-hydroxylase enzyme system. This defects leads to low to unmeasureable plasma Calcitriol levels. Type II rickets occurs secondary to a malfunction in Vitamin D receptors. This malfunction not only stops the receptors from responding to Vitamin D, but also causes high calcitriol concentrations, because there is no feedback control to stop Calcitriol production. Type II rickets has been identified in a small number of cats over the last 15 years. Since Calcitriol assays are not available, these cats are put on high doses of Calcitriol and their Calcium is rechecked in 1-2 weeks. If the Calcium level has not increased, then the presumptive diagnosis is Type II rickets. Treatment involves progressively higher doses of Calcitriol to overwhelm the defective receptors. Oral calcium supplements are also recommended. Kittens that make it out of the active growth phase, can many times live without Calcitriol supplementation, since their adult bodies do not require as efficient calcium handling.

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