Non-Protein Nitrogen substances-NPN
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| Nessler's reagent | convert nitrogen to ammonia which formed a yellow color
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| Berthlot Reaction | Nitroprusside + NH4 = color
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| BUN Blood Urea Nitrogen | major nitrogen-containing metabolic product of protein catabolism in humans
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| How is BUN formed? | Exogenous protein: protein in diet
Endogenous: protein from breakdown of cells in body
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| Where is BUN synthesized? | In the liver from CO2 and ammonia
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| How is ammonia formed? | by the deamination of amino acids during protein catabolism. It is converted to urea.
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| How is urea transported and to where? | carried in blood to the kidney and filtered in the glomerulus
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| How much urea is excreted and reabsorbed? | 60% is excreted and about 40% is reabsorbed
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| What does BUN do? | indicator of renal function/ how well kidneys work
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| Uremia | increased levels of urea in the blood/usually associated with renal failure
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| Azotemia | elevated levels of urea, creatinine and uric acid in the blood
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| Pre-renal | caused by reduced renal blood flow
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| renal | decreased renal function
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| Post-renal | obstruction of the urine flow anywhere in the urinary tract
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| What do high levels of BUN mean? | kidney failure
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| Renal disease | abnormal urea concentrations determined by calculation of the urea/creatinine ratio.
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| Normal urea/creatinine ratio | 10:1 to 20:1
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| Pre-renal disease | high ration/creatinine is normal
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| Post-renal disease | high ration/creatinine is elevated
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| Severe liver disease | low ratio/decreases urea production
BUN levels low
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| BUN-Analytic Methods | conversion factor is calculated using the molecular weight of BUN (60) and nitrogen (28)
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| 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
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| To convert urea nitrogen to urea | the factor is (60/28) or 2.14
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| Diactyl or Fearon reaction | colorimetric reaction/condensation of diacetyl with urea to form the chromogen diazine
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| Enzymatic method | Hydrolysis of urea by urease
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| 2 enzymatic methods | Glutamate dehydrogenase (GLDH) procedure and Nessler's reaction
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| 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
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| Nessler's reaction | The addition of a double iodide compound / results in the formation of a yellow to orange brown compound in NH4
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| Ion selective electrodes | measure the generation of ammonium ions/not a great method
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| Chromogen dyes | pH indictors/ measure the amount of ammonium ions- the more acids the more color
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| BUN Specimen requirements | Serum. DO NOT USE: sodium citrate or sodium fluoride - inhibit urease reaction of analysis. fasting is not required
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| BUN normal ranges | serum: 7-18mg/dl
Urine: 12-20 g/day
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| Creatine | It is synthesized in the liver and transported to tissue (mostly muscle) and converted to phosphocreatine
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| 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.
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| What is creatinine a waste product of? | creatine and creatine phosphate
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| Where is creatinine filtered | glomeruli and does not undergo and significant tubular reabsorption.
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| How is creatinine excreted | in the urine.
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| Disease correlation of elevated creatinine | abnormal renal function / decreased glomerulus filtration rate. GFR= V/T
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| 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
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| Desease correlation of elevated creatine | muscle disease, muscular dystrophy, hyperthyroidism, trauma. NOT RELATED TO RENAL DISEASE. Not commonly tested in lab
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| 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
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| 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
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| Enzymatic reaction | coupled enzymatic methods including: creatinine, sarcosine oxidase, and peroxidase (trinder reaction)
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| Creatinine specimen requirements | plasma, serum, and urine/ DO NOT USE HEMOLYZED AND ICTERIC SAMPLES.
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| Creatinine interfering factors | false elevations from ascorbic acid, glucose, alpha-keto acids, cephalosporins with Jaffee
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| BUN:Cr ratio | 10:0 to 20:0
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| Renal disease (BUN:Cr ratio) | BUN and Cr are both elevated proportionally/ration fall in normal range
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| Prerenal azotemia | high ration >20:1 to 30:1 with high BUN & normal/slightly elevated Cr
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| Postrenal obstruction or Prerenal azotemia or Renal disease | high ratios with an elevated Cr
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| 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
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| uric acid at a pH less than 5.6 | Monosodium urate is the predominant form/excreted through the kidneys and gi tract
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| uric acid at pH greater that 6.4 | urate is insoluable/forms crystals
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| Uric acid - Gout | pain & inflammation of the joints/found in men 30-50/ deposits of sodium urates in connective tissues, primarily joints
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| 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
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| Uric acid - Chronic renal disese | problems with filtration and secretion of uric acid/elevate level
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| Lesch-Nyhan syndrome | genetic disorder in males/absences of the enzyme to biosynthesis purines/increase synthesis of purine nucleotides/increased uric acid
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| Hypouricicemia | decreased uric acid result of liver disease and reabsorption defects
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| Caraway method (uric acid analysis) | oxidation of uric acid with reduction of phosphotungetic acid to tungsten blue/ measures development of blue color/ not sprcific
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| Uricase method (uric acid analysis) | catalyzes the oxidation of uric acid to allatoin/ decrease in absorption at 293nm-directly proportional to concentration.
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| 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
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| Specimen requirements for uric acid analysis | serum, plasma, & urine
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| Interfering substances in uric acid analysis | false decrease: high bilirubin levels with peroxidase methods.
false elevations: salicytate and thiaziades
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| Ammonia results from | deamination of amino acids in the intestinal tracts and during exercise
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| 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
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| Ammonia-disease correlation | high concentration: Encephalopathy, Hepatic failure, Reyes syndrome, and inherited deficiencies of the urea cycle enzmes
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| ammonia - analytic methods | Cation-exchange resin, Enzyme assay (mostly used), Ion selecti electrode
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| 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
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| Ammona sources of error | must eliminate any source of ammonia contamination: smoking, urine, detergents, drugs containing ammonia
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| ammonia normal ranges | plasma
adult: 19-60ml/dl
child:68-136ml/dl
urine 140-1500mg N/day
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| Kidney function | removal of unwanted substances from the plasma/homeostasis/hormonal regulation
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| What is the functional unit of the Kidney? | Nephron
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| What are the 5 functional parts of Nephron? | glomerulus, proximal convoluted tubule, loop of Henle, distal convoluted tubule, collecting duct
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| What are the 3 basic substances that are secreted | urea, creatinine, and uric acid
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| Clearance measurements: creatinine | used to measure clearance/Creatinine clearance/used to determine GFR
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| Clearance measurements: Estimated GFR | calculation based on serum creatinine, age, body size, gender, race
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| Clearance measurements: Urea | does not provide a full clearance assessment/ only 40% reabsorbed
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| Clearance measurements: urine electrophoresis | distinguish between acute glomerular nephropathy and tubular proteinuria/screen for monoclonal and polyclonal globulins
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| B2-microglobulins | High levels indicate cellular turnover: Myeloproliferative anmphoproliferative, inflammation, and renal failure
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| myoglobulin | early indicator of myoglobulin induced acute renal failure, measured by immunoassay. Too big to go through kidney
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| microalbumin | management of diabetes mellitus patients
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| 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
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| urinalysis | detailed, in depth assessment of kidney function
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| glomerular diseases | disorders or diseases that directly damage the renal glomerulus
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| acute glomerularnephritis | rapid on set of symptoms, hematuria, proteinuria, elevated BUN and creatinine, hyaline and granular casts, associated with strep a
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| chronic glomerularnephritis | end stage of persistent glomerular damage/slight proteinuria and hematuria
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| 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
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| 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
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| chronic pyelonephritis | permanent scarring of the renal tubules, can lead to renal failure/ findings: alkaline pH, bacteria, nocturia, polyuria, decreased specific gravity, proteinuria
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| Cystitis | bladder infection characterized by dysuria/findings: small protein, hematuria, absence of cellular casts
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| tubular disease renal tubular acidosis (RTA) | can occur in distal and proximal convulated tubules
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| 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
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| 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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