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fasting hypoglycemia is defined as:
< or equal to 55mg/dL (< or equal to 3.0 mmol/L)
fasting hyperglycemia is defined as:
126 mg/dL (7 mmol/L) or higher
glucose levels in: serum:
72-99 fasting
glucose levels in whole blood:
70-130 mg/dL
glucose levels in CSF:
45-80 mg/dL (60% [ ] of blood)
glucose levels post-prandial:
how to prep for GTT
glucose tolerance test: high carb diet for 3 days, if vomit, stop
CSF for glucose should be:
Analyzed immediatley
when fasting, venous glucose should be ______ higher than capillary and arterial.
5 mg/dL (0.27 mmol/L)
fructosamine test measures :
past 2-3 weeks (glucose)
A1C measures over:
2-3 months
hemolytic anemia will show ______ glycated Hgb b/c directly related to life of RBC
lower
ion-exchange chromatographic methods falsely ____ Hgb A1C due to _____
increased,HgbS
acetone is a product in:
Carb metabolism. if you have an increase in acetone it means you have a carb metab defect.
Benedict's copper reduction test:
detects glucose in urine. subs that reduce copper sulfate to cuprous oxide in prescence of alkali and heat will produce color change confirming - a reducing substances (not specific for glucose)
Glycolysis _____ in a centrifuge
stops
what is elevated post exercise:
lactic acid, elevated pyruvate
how to diagnose lactase def:
H2 breath test
true glucose [ ] in whole blood is fxn of:
HCT: H2O content much higher in plasma than whole blood so ratio of cells/plasma effects glucose resutls
HCT:
volume of RBCs to all other contents in blood
what does sodium fluoride do:
inhibits glycolysis by preventing WBCs consuming (works for short time, not more than hour)
IU of enzyme activity:
1 umol/min
in spectrophotometry, formula for absorbance of sol:
absorbtivity x light path x [ ]
most specific method for glucose in all body fluids uses:
hexokinase which is specific for other isomers of glucose. it measures amount of NADH from reduced NAD
example of glucose-specific colorimetric method?
glucose oxidase
what catalyzes splitting of fructose 1,6 - diphosphate to glyceraldehyde-3-phosphate and dihydroacetone phosphate
aldolase
consistent analytical error with determination of HDL-cholesterol is caused by:
small [ ] of apo B-containing lipoproteins after precipitation.
HDL composed of:
20%lipid, 50%protein
tri 5%, chol 15%, protein 50%
transportation of 60-75% of plasma choesterol is performed by:
LDL
what disease results from familial absence of HDL?
Tangier disease. defect in catabolism of Apo A-1, an essential apoportein for HDL. due to increased HDL catabolism.
if you put lipid profile in fridge over night 4.C what will you see in the morning: hyperlipoproteinemia and lipoprotein lipase def
creamy layer over clear serum. chylomicrons are present as thick layer on top over plasma surface which typifies familial hyperchylomicronemia due to def in lipoprotein lipase activity.
which lipid result woul dbe expected to be falsely elevated on a serum specimen from a non-fasting patient?
triglycerides.
inhertited disease in which near total def of enzy N-acetyl-beta-dexosaminidase A
Tay Sachs this enzy responsible for hydrolysis of the Beta (1,4)- glycosidic bond between N-acetyl galactosamine and galactose in GM2 gangliosidic. Results in excess phospholipid GM2-gagliosie in neurons.
which dyslipidemias are chylomicrons present?
def of lipase. which hydrolyses chylomicrons and triglycerides.
function of VLDL
endogenous triglyceride transport. in endog path, liver makes trigs from carbs and fatty acids. packed in VLDL and takes to circulation.
turbid serum/ or plasma suggests
elevated chylomicrons
lipemic spec separated and frozen at 120C, to test, week later what should done to test again
warmed @ room temp (37C) and mixed.
fast how long for triglyceride spec test?
10-14 hours but shouldn't be
formula for calculation of absorbance with % T of sol?
2 - log (%T)
sub used to estimate serum [ ] of triglycerides by most methods:
glycerol
method for quant of HDL most suited for clinical labs?
uses antibodies or complex agents to mask or consume nonHDL so no seperation req
A1C
glycosylation of valine in polypeptide N-terminus of adult Hgb
prinicple of occult blood test depends on
peroxidase activity of Hgb
Hgb S can be sep from D by
electrophoresis on diff medium (citrate agar gel) and acidic pH (5.9)
electrophoresis @ alkaline pH, which Hgb slowest?
C
fastest Hgb on electrophoresis at alkaline pH
A
Hgb resistant to alkaline denaturation
Hgb F
urobilinogen formed in
intestines
purpose of adding caffine or methyl alcohol in bilirubin determination is:
allow indirect bili to react with color reagent. principle of diazo rxn with conj bili
priniciple of tablet test for bili in urine/feces
chemical coupling of bili with a diazonium salt to form a purple color
plasma hepranized sample for bili ran by Jendrassik-Grof metho and Evelyn-Mallow. 10-20% higher for 2nd , why?
alcohol reagents cause precipitation of proteins and increased background turbidity.
in liver, bilirubin is converted to:
bilirubin diglucuronide
increased conjugated bili major serum component in?
biliary obstruction in adults and intrahepatic biliary atresia in newborns
Crigler-Najjar syndrome
abnormal metabolism of bili due to absence or def in UDP-glucuronyltransferase resulting in increased unconj bili and kernictreus in neonates.
ref ranges for total serum bili and conj
total: 0 - 1.0 mg/dL (0-17.1 umol/L)
conj (direct) : < 0.3
increased AST but almost normal ALK
acute hepatitis
what gives feces its normal color?
urobilin
condition in which erythrocyte protoporhyrin is increased:
iron def anemia
detection of hereditary coproporphyria should include analyse of:
fresh morning urine and delta-amino levulinic acid.
disease is def of ALA syn which catalyzes 1st step of porphyrin synthesis
urine sample for 'porphyrins' includes?
porphyrin and porphobilinogen screen
enz of heme bioisyn inhibited by lead?
porphobilinogen synthase. PBG synthase and ferrochelatase inihibited.
in amniotic fluid, what is used to detect HDNF
absorbance @ 450nm to detect bili
creatinine measured in amniotic fluid to:
rule out urine contamination
most widely used methods of bili measurement based on:
Jendrassik-Grof
in malloy evelyn for bili, reagent reacted with bili to form purple azobilirubin
diazotized sulfanilic acid.
in Jendrossik Groff the green color measured is:
azobilirubin
in Jendrassik_groff, total bili, alkalin tartrate added to;
raise pH to convert azobilirubin from 450- 560 nm. redish-purple chromagen, with similar absorbance as Hgb as other interfering substances to bluish fchromagen with absorbance @ 600nm.
in aminotic fluid, detection of Rh isosensitization is:
measurement @ 450nm "optical density delta 450" is use to detrmine graphical calculation of amt bili in amniotic fluid. max bili in amniotic fluid m=. max bili absorption is 450nm its found in vivo hemolysis like Rh isosensitiation.
conj hyperbili w increased ALKP assocated with?
cholestatic-hepatic biliary obstruction. if ALK is more increased than AST
most specific enz test for acute pancreatitis
lipase. both lipase and amalse used but lipase perisists longer
enz for conversion of starch to glucose and maltase
amazlye (AMS)
results fro acute pancreatisis
increase AMS and LPS but AMS normal in 3 days
AST increased in what diseases
liver ( present in liver, skeletal muscle, and cardiac tissue)
AST catalyzes:
exchange of amine and keto groups b/w alpha-amino and alpha keto acids
ASt and ALT both elevated in?
viral hepatitis.
interference in serum ezy analysis can occur when significant amount of ______ is found in RBCs
AST b/c found in many cells so when hemolysis occurs lots found.
malate dehydrogenase in coupled rxn with AST
oxidizes oxaloacetate to malate in indicator rxn.
AST and ALT can be 100x increase in:
hepatoceullar disorders
mildly increased enzys (AST, etc) can be seen in ;
chronic hepatitis, hemangioma, , obstructive jaundice.
large levels of LD are seen in
pernicious anemia, also seen in renal disease but not as much
enzy in skeletal muscle, heart, brain and high in muscluar distrophy and myocardial infarction
CK creatine kinase.
enzy present in almost all tissues and can be separated by electrophoresis into 5 isoenzymes.
LD
falsely eleveated LD seen in:
hemolyss B/c rbcs have a lot of LD1 and LD2
which isoenzy indicated acute myocardial damage?
CKMB (CK1)
elevated LD4 and LD5 seen in :
liver and skeletal muscle disease.
which enz is increased 1st in Myo infarct
CK (4-6 hours after) peaks at 12-24. and returns to normal in 48 to 72
LD is 12-24 hours after
2 peaks of CK seen with CKMB and CKMM what happend?
myocardial infarction
total increased serum LD activity is specific to:
sensitive but not specific for neoplastic disease
skeletal muscle disease would show increase in?
aldose and CK
in immunoinhibition phase of CKMB procedure what is inactivated?
M subunit
increase in LD1 and LD2 are seen in
hemolytic anemia due to hemolysis
increase in CK and ASt seen in
muscle damage (such as car accident)
increase in GGT and ALP
obstructive jaundice
if ALP asparate aminotransferase, alanine aminotransferase AST, and GGT slightly increased could mean:
chronic hepatitis but can vary
regan isoenzyme:
abnormal ALP isoenzy. carcinoplacental. originates in placenta and seen in lung breast, colon and ovarian cancer. m ost heat stable isoenz.
most heat labile fraction of ALP is from:
bone
most sensitive indicator for liver damage due to ethanol
GGT
holoenzyme
protein portion of enzyme complex
helps determine the presence of seminal fluid
acid phosphatase
Henderson-Hasselbalch eq:
pH = pKa + log [salt]/[acid]