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Quiz 6 - CLLS 302

Non-Protein Nitrogen substances-NPN

QuestionAnswer
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
Created by: pamela18