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chemistryl
Question | Answer |
---|---|
Nitrogenous waste that is excreted by the kidney via | glomerular filtration. |
Tubule reabsorption occurs | 40-60percent, depending on flow rate. |
Urea | important for renal medullary concentration gradient (Na too). |
BUN primarily used as | an indicator of GFR. |
Azotemia | (increased circulating nitrogenous waste, BUN. |
Pre-renal | reduced renal perfusion. |
Renal | primary kidney disease. |
Post-renal | ureter, bladder, urethral obstruction or rupture |
BUN interpreted in light of | urine SG. |
Adequate min SG that is consistently | attained in healthy animal when faced with a need for water conservation. |
Dog SG | > 1030. |
Cat SG | >1035. |
Others SG | > 1025. |
Increased BUN and adequate SG | Renal tubules are concentrating = pre-renal azotemia,Decreased GFR. |
Increased BUN and inadequate SG (isosthenuric1008-1012, concentration of plasma | Primary renal disease suspected. |
Low sensitivity and specificity | BUN. |
3/4 of both kidneys must be non-functional before BUN will | elevate. |
Many other factors influence level of circulating levels of | BUN. |
Production of BUN Primary source is | dietary protein. |
Ingested protein is converted to | ammonia by bacteria in the gut. |
Ammonia diffuses across the gut into | portal circulation and carried to the liver. |
Liver converts ammonia to | urea. |
Minor elevations of BUN | High protein diet,GI hemorrhage acts as a high protein meal. |
Liver disease | Decrease hepatic conversion of ammonia to urea,Low urea and high ammonia seen. |
Portosystemic shunt | Ammonia absorbed by the gut is not carried to the liver. |
Diuresis | Increased glomerular filtration rate. |
Creatinine | By product of muscle metabolism. |
Excreted almost exclusively by glomerular filtration | creatinine. |
No tubule reabsorption | creatinine. |
Like BUN, used to estimate GFR | creatinine. |
Less influenced by non-renal factors then BUN | creatinine. |
Creatinine levels elevated when BUN is normal | Substances known as non-creatinine chromogens are sometimes present in the blood; false elevated levels. |
Creatinine Production related to | muscle metabolism. |
Creatinine is degradation product of | creatine energy source of muscle. |
Freely diffuses out of muscle cells | creatinine. |
Takes creatinine about 4 hours to | equilibrate throughout body BUN about 1,5 hrs. |
Specific Gravity Solute concentration Defined | density of urine/density of water. |
Measured by refractometer | SG. |
SG is a measure of | tubular function. |
Adequate concentration min SG that should occur with | need to conserve. |
Dog sg | > 1030. |
Cat sg | >1035. |
Others sg | > 1025. |
Isosthenuria | SG = 1008-1012. |
SG Solute concentration is similar to | glomerular filtrate. |
No tubular function required | sg. |
Do not describe SG as low or dilute but as | Unconcentrated. |
Hyposthenuria SG = < 1005 Indicates | dilutional function. |
Hepatobiliary system Injury Small animal | ALT, AST. |
Large animal liver | SDH, AST, GGT. |
ALT alanine aminotransferase only | small animal. |
increased serum values indicate cell injury cytosolic enzyme | ALT. |
Dog and Cat ALT primarily from | hepatocytes, muscle can infrequently contribute. |
muscle contains modest amounts of | ALT. |
severe muscle injury eg HBC or congenital myopathies may cause increase | ALT. |
mild to moderate muscle injurty unlikely to cause significant | ALT changes. |
T 1/2 = 2,5 days in dog, 3,5 hours in cat | ALT. |
ALT generally magnitude parallels number of cells affected, not | severity or reversibility. |
AST aspartate aminotransferase both large and small animal | Increased serum levels indicate cell injury cytosolic and mitochondrial. |
AST highest values occur with severe | cellular injury that includes mitochondrial injury. |
High activity in liver and muscle | AST. |
high serum level can result from injury to either organ | AST. |
must be used in combo with other tests ALT, SDH, CK muscle | AST. |
also present in RBC hemolyzed samples can contribute to increase values | AST. |
T 1/2 = < 24 hours in dog and cat,7-10 days in horse | AST. |
SDH sorbitol dehydrogenase large and small increase indicates | hepatocellular injury cytosolic in all species. |
T 1/2 very short minutes to hours | SDH. |
use with other injury enzyme AST having a longer half life | SDH. |
useful to follow progression | SDH. |
helpful to determine if AST is increased because of muscle or liver injury | SDH. |
GGT gamma glutamyltransferase large animal increase mainly due to | chlosestasis but may increase with acute, severe hepatic injury. |
T 1/2 = 3 days in horse | GGT. |
Cholestasis | ALP, GGT, bilirubin, urine bilirubin. |
sensitivity of tests dog | ALP > GGT > urine bilirubin > serum bilirubin. |
ALP alkaline phosphatase inducible enzyme mostly | bound to hepatocellular membranes less in biliary cells chloestais marker. |
T 1/2 dog = 3 days,cat = 6 hours,horse = between dog and cat, but more like cat | ALP. |
Not liver specific | ALP. |
found in liver | hALP, bone bALP, placenta, intestine, kidney, and leukocytes. |
also induced by both endogenous and exogenous corticosteroids | cALP in dog. |
Drugs, steroids and anticuvulsants Phenobarbital | ALP. |
Interpretation of increased ALP- dog general | < 4X increase is non-specific could be from any of the above sources. |
> 4 x increase = cholestasis and/or isoenzyme induction | hALP, cALP. |
ALP 4X increase,3 possibilities | pure cholestasis,pure isoenzyme induction corticosteroids, anticonvulsants,both cholestasis & isoenzyme induction. |
must interpret ALP with other heptobiliary tests | injury, cholestatis, conjugated bilirubin. |
ALP-cat | any increase is significant =cholestasis. |
Cat ALP T 1/2 is | short. |
Feline liver ALP activity is | 3x lower compared to dogs. |
GGT gamma glutamyltransferase | inducible enzyme bound to membranes of bile duct epithelial cells and , to a lesser extent hepatocytes. |
Dogs and cats increased serum levels are liver specific and indicate chlestasis | GGT. |
GGT large animal increase mostly due to | cholestatsis, but may increase with acute, severe injury. |
T 1/2 = 3 days in horses probably in dog and cat | GGT. |
Bilirubin | less sensitive indicators of cholestasis than ALP, GGT. |
Bilirubin Production and excretions produced during | phagocytoses of senescent RBCs. |
hemoglobin converted is converted to | heme and globin. |
globin a protein degreaded to its | amino acid constituents and recycled. |
heme, degraded to free | unconjugated bilirubin. |
Unconjugated bilirubin is complexed with | albumin and carried to liver. |
conjugated by liver with glucuronic acid and excreted in | bile. |
increase in total circulating bilirubin may result from | prehaptic, intrahepatic, or posthepatic causes. |
pre-hepatic = | hemolysis increased RBC breakdown, 75 unconjugated. |
intrahepatic = | both conjugated and unconjugated bilirubin. |
posthepatic = | 75 conjugated bilirubin. |
urine bilirubin only conjugated bilirubin passes the | glomerulus. |
increased urine bilirubin used as indicator for | cholestasis. |
dog normally renal threshold for bilirubin is | low any increase is significant. |
cat high renal threshold urine bilirubin only present in | severe cases of liver disease. |
Decreased Functional Mass loss of functional hepatocytes from severe cirrhosis for example, or from an infiltrative process such as | hepatic lipidosis or neoplasia OR vascular shunt that bypasses hepatocytes. |
at least 70-80 of functional liver mass must be lost before signs and/or functional assays are altered | urine bilirubin. |
decreased BUN as compared to creatinine which is often unaffected, unless animal has | very low muscle mass or medullary washout from low urea, causing increased GFR & low creatinine. |
Can also see Decreased BUN with normal creatinine if | low protein diet or decreased intake, mild anorexia. AMMONIA should be increased along with decreased BUN because of |
dec albumin from dec synthesis OTHER DDx | inflammation mild dec neg acute phase protein,renal loss,intestinal loss panhypoproteinemia,sequestration exudates,inc vascular permeability,peritonitis,3rd space dz. |