Help
Options
Question
Nessler's reagent
click to flip
Didn't know it?
click below
click below
Knew it?
click below
click below
Don't know
Question
Berthlot Reaction
Remaining cards (91)
Know
retry
shuffle
restart
0:00
Embed Code - If you would like this activity on your web page, copy the script below and paste it into your web page.
Normal Size Small Size show me how
Normal Size Small Size show me how
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
Popular Laboratory Science sets