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Non-Protein Nitrogen substances-NPN

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Nessler's reagent   convert nitrogen to ammonia which formed a yellow color  
Berthlot Reaction   Nitroprusside + NH4 = color  
BUN Blood Urea Nitrogen   major nitrogen-containing metabolic product of protein catabolism in humans  
How is BUN formed?   Exogenous protein: protein in diet Endogenous: protein from breakdown of cells in body  
Where is BUN synthesized?   In the liver from CO2 and ammonia  
How is ammonia formed?   by the deamination of amino acids during protein catabolism. It is converted to urea.  
How is urea transported and to where?   carried in blood to the kidney and filtered in the glomerulus  
How much urea is excreted and reabsorbed?   60% is excreted and about 40% is reabsorbed  
What does BUN do?   indicator of renal function/ how well kidneys work  
Uremia   increased levels of urea in the blood/usually associated with renal failure  
Azotemia   elevated levels of urea, creatinine and uric acid in the blood  
Pre-renal   caused by reduced renal blood flow  
renal   decreased renal function  
Post-renal   obstruction of the urine flow anywhere in the urinary tract  
What do high levels of BUN mean?   kidney failure  
Renal disease   abnormal urea concentrations determined by calculation of the urea/creatinine ratio.  
Normal urea/creatinine ratio   10:1 to 20:1  
Pre-renal disease   high ration/creatinine is normal  
Post-renal disease   high ration/creatinine is elevated  
Severe liver disease   low ratio/decreases urea production BUN levels low  
BUN-Analytic Methods   conversion factor is calculated using the molecular weight of BUN (60) and nitrogen (28)  
To convert from urea to urea nitrogen   divide the molecular weight of nitrogen by the molecular weight if urea (28/60) for a factor of 0.467  
To convert urea nitrogen to urea   the factor is (60/28) or 2.14  
Diactyl or Fearon reaction   colorimetric reaction/condensation of diacetyl with urea to form the chromogen diazine  
Enzymatic method   Hydrolysis of urea by urease  
2 enzymatic methods   Glutamate dehydrogenase (GLDH) procedure and Nessler's reaction  
GLDH   oldest method and most common used, standard and least expensive. Often coupled with L-glutamate dehydrogenase to measure the rate of disappearance of NADH  
Nessler's reaction   The addition of a double iodide compound / results in the formation of a yellow to orange brown compound in NH4  
Ion selective electrodes   measure the generation of ammonium ions/not a great method  
Chromogen dyes   pH indictors/ measure the amount of ammonium ions- the more acids the more color  
BUN Specimen requirements   Serum. DO NOT USE: sodium citrate or sodium fluoride - inhibit urease reaction of analysis. fasting is not required  
BUN normal ranges   serum: 7-18mg/dl Urine: 12-20 g/day  
Creatine   It is synthesized in the liver and transported to tissue (mostly muscle) and converted to phosphocreatine  
Creatinine   Synthesized in liver from 3 amino acids (arginine, glycine & methionine). A waste product of creatine and creatine phosphate. Generated through a nonenzymatic irreversible dehydration reaction.  
What is creatinine a waste product of?   creatine and creatine phosphate  
Where is creatinine filtered   glomeruli and does not undergo and significant tubular reabsorption.  
How is creatinine excreted   in the urine.  
Disease correlation of elevated creatinine   abnormal renal function / decreased glomerulus filtration rate. GFR= V/T  
Creatine Clearance Test   The volume of plasma cleared of creatinine per minute per standard body surface/ assessment of GFR. More muscle mass the more creatinine you make  
Desease correlation of elevated creatine   muscle disease, muscular dystrophy, hyperthyroidism, trauma. NOT RELATED TO RENAL DISEASE. Not commonly tested in lab  
Jaffee reaction   End point reaction. Creatinine reacts with picrate ion in alkaline solution, forms a red-orange substance, & measure with a spectrophotometer at 510-520nm. non-specific/many interfering substances  
Kinetic Jaffee   measures the rate of change in absorbance/serum mixed with alkaline picric acid, rate of reaction is measured (color)/fewer interferences/ routinely used  
Enzymatic reaction   coupled enzymatic methods including: creatinine, sarcosine oxidase, and peroxidase (trinder reaction)  
Creatinine specimen requirements   plasma, serum, and urine/ DO NOT USE HEMOLYZED AND ICTERIC SAMPLES.  
Creatinine interfering factors   false elevations from ascorbic acid, glucose, alpha-keto acids, cephalosporins with Jaffee  
BUN:Cr ratio   10:0 to 20:0  
Renal disease (BUN:Cr ratio)   BUN and Cr are both elevated proportionally/ration fall in normal range  
Prerenal azotemia   high ration >20:1 to 30:1 with high BUN & normal/slightly elevated Cr  
Postrenal obstruction or Prerenal azotemia or Renal disease   high ratios with an elevated Cr  
What is uric acid   nitrogenous end product of the catabolism of purines (from dietary & endogenous sources)/primarily occurs in the liver & transported to the kidney via plasma  
uric acid at a pH less than 5.6   Monosodium urate is the predominant form/excreted through the kidneys and gi tract  
uric acid at pH greater that 6.4   urate is insoluable/forms crystals  
Uric acid - Gout   pain & inflammation of the joints/found in men 30-50/ deposits of sodium urates in connective tissues, primarily joints  
Uric acid - Hyperuticemia   overproduction or under excretion f uric acid/increased purine diet or drugs/increased catabolism of nucleic acids of cell nuclei. Found in Chemotherapy  
Uric acid - Chronic renal disese   problems with filtration and secretion of uric acid/elevate level  
Lesch-Nyhan syndrome   genetic disorder in males/absences of the enzyme to biosynthesis purines/increase synthesis of purine nucleotides/increased uric acid  
Hypouricicemia   decreased uric acid result of liver disease and reabsorption defects  
Caraway method (uric acid analysis)   oxidation of uric acid with reduction of phosphotungetic acid to tungsten blue/ measures development of blue color/ not sprcific  
Uricase method (uric acid analysis)   catalyzes the oxidation of uric acid to allatoin/ decrease in absorption at 293nm-directly proportional to concentration.  
Coupled enzyme (uric acid analysis)   decrease in absorbance at 293nm, a peak absorbance for uric acid and 1 at allantoin foes not absorb/peroxidase is a 2nd modification and the most common automated method  
Specimen requirements for uric acid analysis   serum, plasma, & urine  
Interfering substances in uric acid analysis   false decrease: high bilirubin levels with peroxidase methods. false elevations: salicytate and thiaziades  
Ammonia results from   deamination of amino acids in the intestinal tracts and during exercise  
What happens to ammonia   consumed by the parenchymal cells in the prod of urea, exists in the body as ammonium ion- at body pH/not dependent on renal function/measured to confirm the liver'sability to produce ammonia  
Ammonia-disease correlation   high concentration: Encephalopathy, Hepatic failure, Reyes syndrome, and inherited deficiencies of the urea cycle enzmes  
ammonia - analytic methods   Cation-exchange resin, Enzyme assay (mostly used), Ion selecti electrode  
Ammonia specimen requirements   whole blood levels rapidly increase following collection/ specimen should be: placed immediately on ice, centrifuged at 0-4 degrees within 20 minutes of collection, and assayed or frozen asap  
Ammona sources of error   must eliminate any source of ammonia contamination: smoking, urine, detergents, drugs containing ammonia  
ammonia normal ranges   plasma adult: 19-60ml/dl child:68-136ml/dl urine 140-1500mg N/day  
Kidney function   removal of unwanted substances from the plasma/homeostasis/hormonal regulation  
What is the functional unit of the Kidney?   Nephron  
What are the 5 functional parts of Nephron?   glomerulus, proximal convoluted tubule, loop of Henle, distal convoluted tubule, collecting duct  
What are the 3 basic substances that are secreted   urea, creatinine, and uric acid  
Clearance measurements: creatinine   used to measure clearance/Creatinine clearance/used to determine GFR  
Clearance measurements: Estimated GFR   calculation based on serum creatinine, age, body size, gender, race  
Clearance measurements: Urea   does not provide a full clearance assessment/ only 40% reabsorbed  
Clearance measurements: urine electrophoresis   distinguish between acute glomerular nephropathy and tubular proteinuria/screen for monoclonal and polyclonal globulins  
B2-microglobulins   High levels indicate cellular turnover: Myeloproliferative anmphoproliferative, inflammation, and renal failure  
myoglobulin   early indicator of myoglobulin induced acute renal failure, measured by immunoassay. Too big to go through kidney  
microalbumin   management of diabetes mellitus patients  
cystatin C   low molecular protein, produce by nucleated cells, filtered & reabsorbed by glomerulus at a constant rate, assess early changes in kidney function, measured by immunoassay  
urinalysis   detailed, in depth assessment of kidney function  
glomerular diseases   disorders or diseases that directly damage the renal glomerulus  
acute glomerularnephritis   rapid on set of symptoms, hematuria, proteinuria, elevated BUN and creatinine, hyaline and granular casts, associated with strep a  
chronic glomerularnephritis   end stage of persistent glomerular damage/slight proteinuria and hematuria  
Nephrotic syndrome   complication of glomerularnephritis or as a result of circulatory disorders that affect blood pressure or blood flow to kidney/proteinuria, hypoalbuminemia, hyperlipidemia, pitting anemia  
acute pyelonephritis   inflammatory process involving a bacteria infection of the renal rubules by gram- bacteria/usually does not cause permanent damage/common causes: catheterization, urinary obstruction, diabetes  
chronic pyelonephritis   permanent scarring of the renal tubules, can lead to renal failure/ findings: alkaline pH, bacteria, nocturia, polyuria, decreased specific gravity, proteinuria  
Cystitis   bladder infection characterized by dysuria/findings: small protein, hematuria, absence of cellular casts  
tubular disease renal tubular acidosis (RTA)   can occur in distal and proximal convulated tubules  
urinary tract infections/obstructions   infections in the kidney or bladder,bacterial colony count > 10x 3, bacteruria, hematuria & pyuria/obstruction in upper or lower tract/kidney stones  
renal failure   acute: sudden/sharp decline in func./acute toxic or hypoxic insult Chronic: kidney disease, slow decline Diabetes Mellitus: decrease function, 45% of patients with Type 1 diabetes renal hypertension decreased perfusion to all or part of the kidney  


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Created by: pamela18