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Quiz 6 - CLLS 302
Non-Protein Nitrogen substances-NPN
| Question | Answer |
|---|---|
| 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
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