Difference between revisions of "Donkey Biochemistry"

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===Donkey===
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|sublink1= Donkey Section - WikiNormals
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{|border="2" width="800px" align="center" cellspacing="0" cellpadding="4" rules="all" style="margin:1em 1em 1em 0; border:solid 1px #AAAAAA; border-collapse:collapse;empty-cells:show"
 
{|border="2" width="800px" align="center" cellspacing="0" cellpadding="4" rules="all" style="margin:1em 1em 1em 0; border:solid 1px #AAAAAA; border-collapse:collapse;empty-cells:show"
 
!bgcolor="#A7C1F2" width="180px"|Parameter/units
 
!bgcolor="#A7C1F2" width="180px"|Parameter/units
Line 7: Line 14:
 
|-
 
|-
 
!align="left"|Trig mmol/l
 
!align="left"|Trig mmol/l
|1
+
|1.4
|(0.2 - 4.3)
+
|(0.6 - 2.8)
 
|'''Triglyceride'''. Elevations occur in hyperlipaemia.
 
|'''Triglyceride'''. Elevations occur in hyperlipaemia.
 
|-
 
|-
!align="left" bgcolor="#F2F2F2"|CPK IU/l
+
!align="left" bgcolor="#F2F2F2"|CPK iu/l
|bgcolor="#F2F2F2"|97
+
|bgcolor="#F2F2F2"|208
|bgcolor="#F2F2F2"|(36 - 360)
+
|bgcolor="#F2F2F2"|(128 - 525)
 
|bgcolor="#F2F2F2"|'''Creatine phosphokinase'''. Elevations seen in the presence of acute myopathy: Skeletal myopathy, cardiac myopathy and brain pathology.
 
|bgcolor="#F2F2F2"|'''Creatine phosphokinase'''. Elevations seen in the presence of acute myopathy: Skeletal myopathy, cardiac myopathy and brain pathology.
 
|-
 
|-
!align="left"|AST IU/l
+
!align="left"|AST iu/l
|220
+
|362
|(11 - 402)
+
|(238 - 536)
 
|'''Aspartate aminotransferase'''. Elevations seen with acute myopathy or hepatopathy. Elevations in combination with CPK indicate that muscle is the most likely source.
 
|'''Aspartate aminotransferase'''. Elevations seen with acute myopathy or hepatopathy. Elevations in combination with CPK indicate that muscle is the most likely source.
 
|-
 
|-
!align="left" bgcolor="#F2F2F2"|GGT IU/l
+
!align="left" bgcolor="#F2F2F2"|GGT iu/l
|bgcolor="#F2F2F2"|29
+
|bgcolor="#F2F2F2"|24
|bgcolor="#F2F2F2"|(13 - 79)
+
|bgcolor="#F2F2F2"|(14 - 69)
 
|bgcolor="#F2F2F2"|'''Gamma glutamyl transferase.''' Found in hepatocyte and biliary cell membranes, pancreas and the kidney. Elevations are seen in acute hepatitis, chronic liver cirrhosis, chronic pyrrolizidine alkaloid toxicity and rarely with  pancreatitis.
 
|bgcolor="#F2F2F2"|'''Gamma glutamyl transferase.''' Found in hepatocyte and biliary cell membranes, pancreas and the kidney. Elevations are seen in acute hepatitis, chronic liver cirrhosis, chronic pyrrolizidine alkaloid toxicity and rarely with  pancreatitis.
 
|-
 
|-
!align="left"|GLDH IU/l
+
!align="left"|GLDH iu/l
|2.9
+
|2.5
|(0.7 - 14.6)
+
|(1.2 - 8.2)
 
|'''Glutamate dehydrogenase.''' A mitochondrial enzyme; elevations seen with acute hepatocellular damage, and sometimes seen in skin conditions and enteropathy.
 
|'''Glutamate dehydrogenase.''' A mitochondrial enzyme; elevations seen with acute hepatocellular damage, and sometimes seen in skin conditions and enteropathy.
 
|-
 
|-
!align="left" bgcolor="#F2F2F2"|ALP IU/l
+
!align="left" bgcolor="#F2F2F2"|ALP iu/l
|bgcolor="#F2F2F2"|265
+
|bgcolor="#F2F2F2"|152
|bgcolor="#F2F2F2"|(110 - 563)
+
|bgcolor="#F2F2F2"|(98 - 252)
 
|bgcolor="#F2F2F2"|'''Alkaline phosphatase.''' A brush border enzyme; elevations are seen in chronic biliary obstructive liver pathology, abnormalities of bone metabolism and intestinal disease.
 
|bgcolor="#F2F2F2"|'''Alkaline phosphatase.''' A brush border enzyme; elevations are seen in chronic biliary obstructive liver pathology, abnormalities of bone metabolism and intestinal disease.
 
|-
 
|-
!align="left"|Bile acids
+
!align="left"|Bile acids μmol/l
|<20
+
|10
|.
+
|(2.6 - 18.6)
 
|Elevations occur with impaired hepatobiliary function such as cholelithiasis, acute hepatitis, chronic liver cirrhosis, and chronic pyrrolizidine alkaloid toxicity. May sometimes be seen with hyperlipaemia, malignant lymphoma and toxic myopathy.
 
|Elevations occur with impaired hepatobiliary function such as cholelithiasis, acute hepatitis, chronic liver cirrhosis, and chronic pyrrolizidine alkaloid toxicity. May sometimes be seen with hyperlipaemia, malignant lymphoma and toxic myopathy.
 
|-
 
|-
 
!align="left" bgcolor="#F2F2F2"|Tbil μmol/l
 
!align="left" bgcolor="#F2F2F2"|Tbil μmol/l
|bgcolor="#F2F2F2"|2.7
+
|bgcolor="#F2F2F2"|1.6
|bgcolor="#F2F2F2"|(1.4 - 7.7)
+
|bgcolor="#F2F2F2"|(0.1 - 3.7)
 
|bgcolor="#F2F2F2"|'''Total bilirubin.''' Increases may be difficult to interpret without clinical disease. Levels can increase with anorexia and intestinal malfunction.
 
|bgcolor="#F2F2F2"|'''Total bilirubin.''' Increases may be difficult to interpret without clinical disease. Levels can increase with anorexia and intestinal malfunction.
 
|-
 
|-
 
!align="left"|TP g/l
 
!align="left"|TP g/l
|70
+
|65
|(58 - 82)
+
|(58 - 76)
 
|'''Total protein'''. Composed of albumin and globulins. Elevations seen with dehydration, inflammation and myeloma. Decreases may be seen with renal and gastrointestinal disease (loss), hepatic disease and starvation (reduced production).
 
|'''Total protein'''. Composed of albumin and globulins. Elevations seen with dehydration, inflammation and myeloma. Decreases may be seen with renal and gastrointestinal disease (loss), hepatic disease and starvation (reduced production).
 
|-
 
|-
 
!align="left" bgcolor="#F2F2F2"|Alb g/l
 
!align="left" bgcolor="#F2F2F2"|Alb g/l
|bgcolor="#F2F2F2"|28
+
|bgcolor="#F2F2F2"|26
|bgcolor="#F2F2F2"|(20 - 34)
+
|bgcolor="#F2F2F2"|(22 - 32)
 
|bgcolor="#F2F2F2"|'''Albumin.''' Hypoalbuminaemia may be seen with decreased synthesis resulting from intestinal malabsorption, malnutrition, chronic inflammatory disease and chronic liver disease. It is lost in renal disease and gastrointestinal disease.
 
|bgcolor="#F2F2F2"|'''Albumin.''' Hypoalbuminaemia may be seen with decreased synthesis resulting from intestinal malabsorption, malnutrition, chronic inflammatory disease and chronic liver disease. It is lost in renal disease and gastrointestinal disease.
Hypoalbuminaemia occurs only in severe dehydration.
+
Hyperalbuminaemia occurs only in severe dehydration.
 +
|-
 +
!align="left"|Glob g/l
 +
|38
 +
|(32 - 48)
 +
|'''Globulins.''' Acute phase proteins. Inflammatory processes usually result in increases in globulins. Serum protein electrophoresis is rarely indicated except in the investigation of certain neoplastic processes. Hypoglobulinaemia may be seen subsequent to infectious disease processes but is rarely of relevance. Hyperglobulinaemia may also be seen in cases of hepatopathy.
 +
|-
 +
!align="left" bgcolor="#F2F2F2"|Creat μmol/l
 +
|bgcolor="#F2F2F2"|87
 +
|bgcolor="#F2F2F2"|(53 - 118)
 +
|bgcolor="#F2F2F2"| '''Creatinine.''' Produced in the body by muscle breakdown and filtered by the kidneys. A marker of renal function. In equines creatinine is the most reliable marker of glomerular filtration rate as tubular reabsorption is minimal. Renal tubular damage and reduced glomerular filtration rates will result in increased creatinine.
 +
|-
 +
!align="left"|Urea mmol/l
 +
|3.2
 +
|(1.5 – 5.2)
 +
|'''Urea.''' Relevant to renal and hepatic function. Traditionally used as a marker of glomerular filtration rate but is subject to enterohepatic recycling and has variable reabsorption in the renal tubules. Elevations in creatinine due to renal dysfunction are more reliable than changes in urea.
 +
Urea is produced in the liver. Reduced hepatic function may result in decreases in urea.
 +
|-
 +
!align="left" bgcolor="#F2F2F2"|Amylase iu/l
 +
|bgcolor="#F2F2F2"|4
 +
|bgcolor="#F2F2F2"|(1 - 10.6)
 +
|bgcolor="#F2F2F2"|Elevations occur with pancreatitis.
 
|-
 
|-
!align="left"|Amylase IU/l
+
!align="left" |Lipase iu/l
|8
+
|12.9
|(0 - 24)
+
|(7.8 - 27.3)
 
|Elevations occur with pancreatitis.
 
|Elevations occur with pancreatitis.
 
|-
 
|-
!align="left" bgcolor="#F2F2F2"|Lipase IU/l
+
!align="left" bgcolor="#F2F2F2"|Glucose mmol/l
|bgcolor="#F2F2F2"|16
+
| bgcolor="#F2F2F2"|4.43
|bgcolor="#F2F2F2"|(1 - 66)
+
| bgcolor="#F2F2F2"| (3.9 - 4.7)
|bgcolor="#F2F2F2"|Elevations occur with pancreatitis.
+
| bgcolor="#F2F2F2"|Blood '''glucose''' concentration is related to diet, insulin, glucagon and body requirement. Prolonged hyperglycaemia is seen in hyperadrenocorticism and pituitary adenoma. A transient hyperglycaemia occurs postprandially and with stress. Hypoglycaemia can be seen in liver failure, septicaemia, malabsorption and starvation. Can be used for the diagnosis of intestinal  malabsorption. False reductions in serum glucose may occur in vitro due to glycolysis by erythrocytes.
 
|-
 
|-
!align="left"|Glucose mmol/l
+
!align="left" |Calcium mmol/l
|.
+
|3
|(3.1 - 5)
+
|(2.2 – 3.4)
|Blood '''glucose''' concentration is related to diet, insulin, glucagon and body requirement. Prolonged hyperglycaemia is seen in hyperadrenocorticism and pituitary adenoma. A transient hyperglycaemia occurs postprandially and with stress. Hypoglycaemia can be seen in liver failure, septicaemia, malabsorption and starvation. Can be used for the diagnosis of intestinal  malabsorption. False reductions in serum glucose may occur in vitro due to glycolysis by erythrocytes.
+
|Elevations occur with pancreatitis.
 
|-
 
|-
 +
 
!align="left" bgcolor="#F2F2F2"|Na mmol/l
 
!align="left" bgcolor="#F2F2F2"|Na mmol/l
|bgcolor="#F2F2F2"|.
+
|bgcolor="#F2F2F2"|133
|bgcolor="#F2F2F2"|(130 - 149)
+
|bgcolor="#F2F2F2"|(128 - 138)
 
|bgcolor="#F2F2F2"|'''Sodium.''' Hypernatremia may be seen in dehydration and salt poisoning. Hyponatraemia can occur with  diarrhoea, adrenal insufficiency, renal disease, excessive sweating or sequestration of fluid. Hyponatraemia with hyperkalemia may
 
|bgcolor="#F2F2F2"|'''Sodium.''' Hypernatremia may be seen in dehydration and salt poisoning. Hyponatraemia can occur with  diarrhoea, adrenal insufficiency, renal disease, excessive sweating or sequestration of fluid. Hyponatraemia with hyperkalemia may
 
occur in uroperitoneum and hypoadrenocorticism.
 
occur in uroperitoneum and hypoadrenocorticism.
 
|-
 
|-
 
!align="left"|K mmol/l
 
!align="left"|K mmol/l
|.
+
|4.3
|(2.8 - 4.3)
+
|(3.2 - 5.1)
 
|Serum '''potassium''' is not a reliable indicator of total body potassium as concentrations vary between the intracellular and extracellular fluid, and values should be interpreted in conjunction with blood pH. Hyperkalemia can occur with tissue necrosis, strenuous exercise, acidemia, uroperitoneum, hypoadrenocorticism and artefactually with erythrocyte haemolysis. Hypokalemia can occur with anorexia, excess sweating, urinary and gastrointestinal loss.
 
|Serum '''potassium''' is not a reliable indicator of total body potassium as concentrations vary between the intracellular and extracellular fluid, and values should be interpreted in conjunction with blood pH. Hyperkalemia can occur with tissue necrosis, strenuous exercise, acidemia, uroperitoneum, hypoadrenocorticism and artefactually with erythrocyte haemolysis. Hypokalemia can occur with anorexia, excess sweating, urinary and gastrointestinal loss.
 
|-
 
|-
 
!align="left" bgcolor="#F2F2F2"|Cl mmol/l
 
!align="left" bgcolor="#F2F2F2"|Cl mmol/l
|bgcolor="#F2F2F2"|.
+
|bgcolor="#F2F2F2"|102
|bgcolor="#F2F2F2"|(95 - 108)
+
|bgcolor="#F2F2F2"|(96 - 106)
 
|bgcolor="#F2F2F2"|Changes in '''chloride''' concentration may accompany changes in sodium concentration, and vary inversely with bicarbonate concentration. Hypochloridemia can result from loss of gastric HCl ''e.g.'' in obstruction of the small intestine, and
 
|bgcolor="#F2F2F2"|Changes in '''chloride''' concentration may accompany changes in sodium concentration, and vary inversely with bicarbonate concentration. Hypochloridemia can result from loss of gastric HCl ''e.g.'' in obstruction of the small intestine, and
 
anterior enteritis. It may also occur with loss of colonic Cl ''e.g.'' in colitis.
 
anterior enteritis. It may also occur with loss of colonic Cl ''e.g.'' in colitis.
 
|-
 
|-
 
!align="left"|Chol mmol/l
 
!align="left"|Chol mmol/l
|.
+
|2.0
|(1 - 3)
+
|(1.4 - 2.9)
 
|Elevations in '''cholesterol''' can occur if there is abnormal lipid metabolism and hyperlipaemia.
 
|Elevations in '''cholesterol''' can occur if there is abnormal lipid metabolism and hyperlipaemia.
 
|-
 
|-
 
|}
 
|}
* Svendsen, E.D., Duncan, J. and Hadrill, D. (2008) ''The Professional Handbook of the Donkey'', 4th edition, Whittet Books, Appendix 1
+
Burden, F.A., Hazell-Smith, E., Mulugeta, G.,  Patrick, V., Trawford, R., Brooks Brownlie, H. (2015). [http://onlinelibrary.wiley.com/doi/10.1111/eve.12512/pdf Reference intervals for biochemical and haematological parameters in mature domestic donkeys (Equus asinus) in the UK.] ''Equine Veterinary Education'', '''28''' (3), 134-139
 +
 
  
 +
{{infotable
 +
|Maintitle = [[Sponsors#The Donkey Sanctuary|This section was sponsored and content provided by '''THE DONKEY SANCTUARY''']]
 +
|Maintitlebackcolour = B4CDCD
 +
}}
 +
[[Category:Donkey]]
  
[[Category:Normal Biochemistry]]
+
[[Category:Biochemistry Reference Ranges]]
 
[[Category:WikiNormals]]
 
[[Category:WikiNormals]]

Latest revision as of 11:57, 23 December 2016

WikiNormalsWikiNormals Banner.png
WIKINORMALS
DONKEY SECTION


Parameter/units Average Range Interpretation
Trig mmol/l 1.4 (0.6 - 2.8) Triglyceride. Elevations occur in hyperlipaemia.
CPK iu/l 208 (128 - 525) Creatine phosphokinase. Elevations seen in the presence of acute myopathy: Skeletal myopathy, cardiac myopathy and brain pathology.
AST iu/l 362 (238 - 536) Aspartate aminotransferase. Elevations seen with acute myopathy or hepatopathy. Elevations in combination with CPK indicate that muscle is the most likely source.
GGT iu/l 24 (14 - 69) Gamma glutamyl transferase. Found in hepatocyte and biliary cell membranes, pancreas and the kidney. Elevations are seen in acute hepatitis, chronic liver cirrhosis, chronic pyrrolizidine alkaloid toxicity and rarely with pancreatitis.
GLDH iu/l 2.5 (1.2 - 8.2) Glutamate dehydrogenase. A mitochondrial enzyme; elevations seen with acute hepatocellular damage, and sometimes seen in skin conditions and enteropathy.
ALP iu/l 152 (98 - 252) Alkaline phosphatase. A brush border enzyme; elevations are seen in chronic biliary obstructive liver pathology, abnormalities of bone metabolism and intestinal disease.
Bile acids μmol/l 10 (2.6 - 18.6) Elevations occur with impaired hepatobiliary function such as cholelithiasis, acute hepatitis, chronic liver cirrhosis, and chronic pyrrolizidine alkaloid toxicity. May sometimes be seen with hyperlipaemia, malignant lymphoma and toxic myopathy.
Tbil μmol/l 1.6 (0.1 - 3.7) Total bilirubin. Increases may be difficult to interpret without clinical disease. Levels can increase with anorexia and intestinal malfunction.
TP g/l 65 (58 - 76) Total protein. Composed of albumin and globulins. Elevations seen with dehydration, inflammation and myeloma. Decreases may be seen with renal and gastrointestinal disease (loss), hepatic disease and starvation (reduced production).
Alb g/l 26 (22 - 32) Albumin. Hypoalbuminaemia may be seen with decreased synthesis resulting from intestinal malabsorption, malnutrition, chronic inflammatory disease and chronic liver disease. It is lost in renal disease and gastrointestinal disease.

Hyperalbuminaemia occurs only in severe dehydration.

Glob g/l 38 (32 - 48) Globulins. Acute phase proteins. Inflammatory processes usually result in increases in globulins. Serum protein electrophoresis is rarely indicated except in the investigation of certain neoplastic processes. Hypoglobulinaemia may be seen subsequent to infectious disease processes but is rarely of relevance. Hyperglobulinaemia may also be seen in cases of hepatopathy.
Creat μmol/l 87 (53 - 118) Creatinine. Produced in the body by muscle breakdown and filtered by the kidneys. A marker of renal function. In equines creatinine is the most reliable marker of glomerular filtration rate as tubular reabsorption is minimal. Renal tubular damage and reduced glomerular filtration rates will result in increased creatinine.
Urea mmol/l 3.2 (1.5 – 5.2) Urea. Relevant to renal and hepatic function. Traditionally used as a marker of glomerular filtration rate but is subject to enterohepatic recycling and has variable reabsorption in the renal tubules. Elevations in creatinine due to renal dysfunction are more reliable than changes in urea.

Urea is produced in the liver. Reduced hepatic function may result in decreases in urea.

Amylase iu/l 4 (1 - 10.6) Elevations occur with pancreatitis.
Lipase iu/l 12.9 (7.8 - 27.3) Elevations occur with pancreatitis.
Glucose mmol/l 4.43 (3.9 - 4.7) Blood glucose concentration is related to diet, insulin, glucagon and body requirement. Prolonged hyperglycaemia is seen in hyperadrenocorticism and pituitary adenoma. A transient hyperglycaemia occurs postprandially and with stress. Hypoglycaemia can be seen in liver failure, septicaemia, malabsorption and starvation. Can be used for the diagnosis of intestinal malabsorption. False reductions in serum glucose may occur in vitro due to glycolysis by erythrocytes.
Calcium mmol/l 3 (2.2 – 3.4) Elevations occur with pancreatitis.
Na mmol/l 133 (128 - 138) Sodium. Hypernatremia may be seen in dehydration and salt poisoning. Hyponatraemia can occur with diarrhoea, adrenal insufficiency, renal disease, excessive sweating or sequestration of fluid. Hyponatraemia with hyperkalemia may

occur in uroperitoneum and hypoadrenocorticism.

K mmol/l 4.3 (3.2 - 5.1) Serum potassium is not a reliable indicator of total body potassium as concentrations vary between the intracellular and extracellular fluid, and values should be interpreted in conjunction with blood pH. Hyperkalemia can occur with tissue necrosis, strenuous exercise, acidemia, uroperitoneum, hypoadrenocorticism and artefactually with erythrocyte haemolysis. Hypokalemia can occur with anorexia, excess sweating, urinary and gastrointestinal loss.
Cl mmol/l 102 (96 - 106) Changes in chloride concentration may accompany changes in sodium concentration, and vary inversely with bicarbonate concentration. Hypochloridemia can result from loss of gastric HCl e.g. in obstruction of the small intestine, and

anterior enteritis. It may also occur with loss of colonic Cl e.g. in colitis.

Chol mmol/l 2.0 (1.4 - 2.9) Elevations in cholesterol can occur if there is abnormal lipid metabolism and hyperlipaemia.

Burden, F.A., Hazell-Smith, E., Mulugeta, G., Patrick, V., Trawford, R., Brooks Brownlie, H. (2015). Reference intervals for biochemical and haematological parameters in mature domestic donkeys (Equus asinus) in the UK. Equine Veterinary Education, 28 (3), 134-139


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