25/26 - Basic Clinical LABS Flashcards
Why are Labs Ordered?
To Confirm a DIAGNOSIS
or to distinguish amoung different forms of a disease/pathology
To assess the severity of a condition
To monitor progress / therapy
To detect side-effects / complications
Typical Labs ordered in an ANNUAL CHECKUP
CBC
Lipid + Glucose Panel
Liver Fxn Panel
Blood tests for kidney fxn
Urinalysis
Thyroid / C-reactive Protein / HbA1C
Vitamin D / Homocysteine / PSA
CBC
Typical Lab ordered for Annual Checkup
Complete Blood Count
includes:
WBC / RBC
WBC differential
Hematocrit / Hemogloblin
Platelet Count
Lipid + Glucose Panel
Typical Lab ordered for Annual Checkup
Total Cholesterol
LDL + HDL
LDL/HDL Ratio
Glucose
Liver (Hepatic) Function Panel
Typical Lab ordered for Annual Checkup
blood levels of:
Total Protein
Albumin / Bilirubin
Liver Enzymes
Blood tests for KIDNEY FUNCTION
Typical Lab ordered for Annual Checkup
Serum CREATININE
- *BUN**
- *blood urea nitrogen**
Urinalysis
Typical Lab ordered for Annual Checkup
Examine specimen for:
color / clarity / odor / pH / spgr
protein / glucose / ketones
Also microscopic analysis for:
bacteria / crystals / blood cells
Assays for VITAMIN status Focus on:
DIRECT measurement of the
vitamin / cofactor / precursor
in biological fluids or blood cells
or measurement of:
Urinary Metabolites
Biochemical Function
that requires the vitamin / cofactor
ex. G6P for thiamine deficiency
Vitamin A
How is it clinically assayed?
Fat Soluble
Vision / growth / Reproduction
night blindness
Fluorometric
HPLC / RIA
Photometric
Fat Soluble Vitamins
How are they clinically assayed?
(ADEK)
HPLC for ALL of them
- RIA** for all except *vitamin E
- not used much anymore due to cost / hazard / license*
Photometric for all except vitamin D
Vitamin D
How is it clinically assayed?
Fat soluble vitamin
Ca2+ metabolism / bones / teeth
rickets / osteomalacia
Competitive Binding Protein = CPB
HPLC / RIA
no photometric assay
Vitamin E
How is it clinically assayed?
Fat-soluble Vitamin
Antioxidant for unsat-lipids
lipid peroxidation / fragile RBC
Erythrocyte Hemolysis
HPLC, NOT RIA
Photometric
Vitamin K
How is it clinically assayed?
Fat-Soluble Vitamin
blood clotting / osteocalcins
increased clotting time + hemorrhages
ProThrombin Time
HPLC / RIA
Photometric
Thiamine
Water Soluble Vitamin, how is it CLINICALLY ASSAYED?
- *B1**
- beri beri*
HPLC / Fluorometric / microbial
Transketolase
Riboflavin
Water Soluble Vitamin, how is it CLINICALLY ASSAYED?
B2
redox / dermatitis, photophobia
Enzyme
HPLC / Fluorometric / Microbial
Pyridoxine
Water Soluble Vitamin, how is it CLINICALLY ASSAYED?
B6
AA + phospholipid metabolism / anemia + convulsions
Tyrosine Decarboxylase
HPLC / no fluoro / Microbial
Niacin
Water Soluble Vitamin, how is it CLINICALLY ASSAYED?
B3
REDOX / pellagra
Fluorometric / Microbial
no HPLC, too common in the immune system
Folate
Water Soluble Vitamin, how is it CLINICALLY ASSAYED?
B9
synthesis of Nucleic+Amino Acids / megaloblastic ANEMIA
same assays as B12
IMMUNOASSAY
CPB = competitive protein binding
no HPLC, common in immune system / no fluoro
Microbial
Cyanobalamin
Water Soluble Vitamin, how is it CLINICALLY ASSAYED?
B12
AA + Lipid metabolism / Pernicious+megaloblastic ANEMIA
same assays as B9, folate
IMMUNOASSAY
CPB = competitive protein binding
- *Microbial**
- no HPLC, common in immune system / no fluoro*
Biotin
Water Soluble Vitamin, how is it CLINICALLY ASSAYED?
B7
Carboxylation / dermatitis
AVIDIN BINDING
Enzymes
PHOTOmetric
Microbial
Pantothenic Acid
Water Soluble Vitamin, how is it CLINICALLY ASSAYED?
B5
Central metabolism / burning feet syndrome
Enzymes
CPB
PHOTOmetric
Microbial
Ascorbate
Water Soluble Vitamin, how is it CLINICALLY ASSAYED?
C
connective tissue / scurvy
PHOTOmetric
HPLC
What Vitamin can be analyzed by
Erythrocyte Hemolysis?
Vitamin E
antioxidant / lipid peroxidation
Which Vitamin can be analyzed by
PROTHROMBIN TIME?
Vitamin K
blood clotting / hemorrhages
Which vitamins can be analyzed by
IMMUNOASSAY?
FOLATE + Cyanobalamin
B9 / B12
both also CPB & Microbial assays
Which vitamin can be analyzed by
AVIDIN BINDING?
BIOTIN
B7
carboxylation / dermatitis
Oral Glucose Tolerance Test
What is done prior / during the test?
OGTT
Controlled diet for 3 days prior to test
After an overnight fast, patient is to swallow a solution with
75 grams of glucose
Then blood samples are drawn at regular intervals and
assayed for glucose
Oral Glucose Tolerance Test
What does it measure?
What is a normal response?
Use a BLOOD DRAW to measure
Glucose concentration over time, after the OGTT load
Normal Response
Peak @30 min,
return to fasting @2hours
fasting = 700-1050 mg/L
OGTT
What is a Diabetic/abnormal Response?
What values indicates Diabetes?
in an abnormal diabetic response,
BOTH Starting Glucose & Glucose PEAK is HIGHER
slow return to fasting level,
or not dropping to NORMAL fasting (700-1050mg/L)
- *DIABETES**
- *> 2000 mg/L**, after 2 hours after the OGTT load
Main differences in clinical test results for
Diabetic vs Non-diabetic
- *DIABETES**
- *>** 2000 mg/L, 2hours post OGTT
- *LATER & HIGHER Peak**
- *Fasting level is also HIGHER**
Normal / Non-diabetic:
Peak @ 30 min
Return to fasting @ 2 hours, (normal = 700-1050 mg/L)
Why do we NOT use urinary glucose levels?
Why is BLOOD GLUCOSE preferred?
The fasting blood glucose level can be measured easily with little interference, and it correlates well with the severity of the disease.
In healthy individuals, Glucose MUST exceed >1800 mg/L
before excessive glucose appears in the urine
In Diabetic patients, the renal threshhold can increase to >3000mg/L
Urinary glucose is NOT a sensitive marker
- Also, excessive glucose excretion can be caused by:*
- *Pregnancy / Rickets / Osteomalacia**
What is often shown in PREDIABETES?
- *IFG_ and/or _IGT**
- AT RISK for T2DM* + stroke + heart attacks
IMPAIRED FASTING GLUCOSE
FBG = 1000-1250 mg/L
>1260 mg/L is diabetes
IMPAIRED GLUCOSE TOLERANCE
blood glucose level is 1400-2000 mg/L
AFTER a 2-hour OGTT
>2000 is diabetes
3 Ways to DIAGNOSE DM by blood glucose levels
What levels?
Tests should be CONFIRMED on a SUBSEQUENT DAY
1) FPG > 1260 mg/L
* (prediabetes = 1000-1250)*
2) Casual plasma BG> 2000 mg/L
3) 2hr OGTT w/ post load value > 2000 mg/L
What are the 3 Ketone Bodies?
involved in KETOSIS
Acetone
B-hydroxybutyrate
Acetoacetate
Organic acids, if their levels rise TOO HIGH –> blood pH = ACIDIC
At what LEVELS is KETOSIS seen?
What symptoms are seen?
Seen with levels of 30-70 mmol/L
Acetone on the breath may be detectible
When does Acidotic Ketosis occur?
when the Blood pH DROPS BELOW 7.3
B-hydroxbutyrate + acetoacetate
Organic acid, concentrations are TOO HIGH
overcome the buffering action of the serum
What are the 2 TYPES of
BLOOD GLUCOSE METERS?
and what do they measure?
FIrst we need to get a single drop of blood, from FINGERSTICK
Electrochemical Glucose monitor
uses glucose oxidase -> hydrogen peroxide -> o2
small electrical current
Photometric Glucose Monitor
similar to above, but color change is measured
What does HbA1c measure?
And how is it correlated with Diabetes?
AVERAGE BG over the last 2-3 Months
HIGH HbA1c : directly proportional to : degree of HYPERglycemia
indicates a loss of BG control or pt’s compliance
assayed by:
electrophoresis
ion exchange / afffinity chromatography
What is NITROGEN BALANCE?
24-hour urine collection used to measure
What are its Positive / Negative values?
Dietary Nitrogen INTAKE - Excretion or Losses
(mainly from AA’s in protein) - (mainly from URINE)
Positive Value = Growth + Development + Pregnancy
- Negative Value = INCREASED catabolism of AA’s + Purines*
- may call for dietary intervention*
Where are AA’s filtered out from?
What occurs if the transport is saturated or defective?
AA’s are filtered in the KIDNEY,
reabsorbed in renal tubules by saturable/active transport systems
If this system is saturated or defective,
the AA’s are left in the urine and are excreted
AMINOACIDURIA
results
What causes PRIMARY Acidurias?
MUTATIONS IN ENZYMES
that are involved in AA metabolism
loss in activity of enzyme –> RAISES concentration of precursors
which will appear in the urine
What is SECONDARY Aciduria?
DAMAGE TO KIDNEY
from various causes:
Viral infection / APAP toxicity / Rickets
Genetic defects in enzyme/transporters in kidney
What are SCREENING TESTS for
Aminoacidurias?
Screening Tests
cheap & fast, not quantitative
specimen can come from urine / blood / CSF
TLC w/ ninhydrin spray
Photometric (UV absorbance)
Guthrie (microbiological)
FeCl3 test for PKU
What are QUANTITATIVE TESTS
for AminoAcidurias?
Quantitiative Tests
slower, not so cheap + needs special equipment
may use urine or blood w/ pre-treatment
HPLC + Ion-Exchange Chromatography
detection by UV / MS for liquid chromatographic methods
Capillary Electrophoresis
UV / MS detection
OTHER Organic ACIDURIAS
other secondary metabolites
Diabetes & Ketone bodies = Acetoacetate + B-hydroxybutyrate
Defects in propionate metabolism
B12 deficiency -> HIGH levels of propionate + methylalonate
- *MSUD** = maple syrup urine disease
- defect in AA metabolism* -> high levels of certain KETO ACIDS
What type of Analysis/Test is done for
VOLATILE ANYLYTES?
GC / MC
for small volatile analytes = you can SMELL IT
Ex. Maple Syrup - MSUD
NOT used for amino Acids
What are anlytes for KIDNEY FUNCTION TESTS?
Where do the specimens come from?
URINE / BLOOD / SERUM
Analytes:
UREA / Uric Acid + Urate / AMMONIA
CREATINE + CREATININE
High capacity of kidney for filtration -> waste products are not seen
until renal function is GREATLY compromised:
Major function of kidney is elimination of nitrogenous wastes
urea / ammonia / urate
What levels/tests are used to monitor the
filtration ability of the KIDNEY?
BUN** (blood urea nitrogen) & **URINARY CREATININE
Nitrogen:Creatinine Ratio is typically 10:1 or 20:1
HIGH RATIO = decreased renal perfusion
cardiac failure / GI bleeding / excess protein / drugs
Low Ratio does not indicate pathology
found with low protein intake
but also with SEVERE LIVER DISEASE
What ORGAN(S) do UREA LEVELS track the health of?
BOTH
LIVER + KIDNEY
Synthesis is in the liver
Excretion is through the kidney
Urea is the MAJOR route by which we excrete NITROGEN
How do we clinically ASSAY
UREA?
Urea + urease -> Ammonia:
Berthelot
ammonia + phonol -> measure absorbance @ 560nm
- *Glutamate dehydrogenase**
- *UV absorbance @ 340nm**
Alternate CHEMICAL method
DIRECT reaction with diacetyl –> DIAZINE
Buttery smell = diacetyl
What are physiological sources of
AMMONIA?
GI TRACT is the main source
NH3 is generated by bacterial action
(proteases / ureases / amine oxidases)
- Some is made by the URIC ACID CYCLE*
- unless there is a defect*
HYPER-Ammonemia
Causes / Effects
Caused by:
- *Inherited Deficiencies** in UREA CYCLE ENZYMES
- *Liver Disease** or Renal Failure
- though the MAJOR source of ammonia is the GI TRACT*
High Ammonia = Toxic, depletes TCA cycle & reduce energy
Nerve Cell damage -> Nausea / Coma / Death
How is Ammonia Analyzed / tested for?
SERUM samples are preferred
Quantitative Methods:
- *Glutamate Dehydrogenase** = PREFERRED
- *Berthelot Method**
Special precautions to avoid CONTAMINATION from:
poor ventilation / smoking residue
poor venipuncture technique
delays in specimin analysis –> degradation
Creatine vs CreaTINine
Creatine –> CreaTINine
SPONTANEOUSLY CONVERTED at a constat rate in the Muscle
reflects the amount of muscle tissue
Creatine + Creatine Kinase -> Phosphocreatine
Phosphocreatine is also converted to CreaTINine
imortant in restoring ENERGY
What does CreaTINine clearance reflect?
What organ?
CrCl
Reflects the ability of the KIDNEY to
FILTER metabolic byproducts from the BLOOD
How is Creatine / CreaTINine Analyzed/Assayed?
Specimen = Serum / Plasma
CreaTINine reacts w/ alkaline picrate –> orange-red complex
measured spectrophometrically
Also enzymatic methods, creaTINine -> creatine ->
color change or UV abosorbance change
or algorithim to compare with measured GFR
24 hour urine collection is ideal, but 12 is fine
How is Uric Acid (Urate) produced?
what does it do?
- *Catabolism of PURINES** = Adenosine & Guanine
- minor source is from DIETARY PURINES*
Uric Acid is excreted through kidney –> urine
in VIVO it is an antioxidant, but will precipitate <5.6 pH
GOUT
poor circulation etc.
What is HYPER-Uricemia?
What diseases does it cause?
Serum / plasma level of urate > 7.0 mg/dL for men >6.0 for women
GOUT
due to urate precipitation in JOINTS
Lesch-Hyhan Syndrome
deficiency in HGPRT enzyme & blocks purine solvage
HIGH levels of hypoxanthine + guanine –> hyperuricemia
How is Urate/Uric Acid Clinically ASSAYED?
HPLC
Phosphotungstic Acid = PTA
BLUE color as PTA is reduced by urate
Uricase
UV absorbance as enzyme, urea -> allotoin
Dry chemistry systems
Sketch the transport of LIPIDS
throughout the BODY
What is the role of Lipoproteins?
Lipoproteins transport LIPIDS through circulation
in micelllular-like complexes
specialized system of lipoproteins & receptors
Body fat is mainly composed of
triglycerides = major long term energy storage
TG / Cholesterol form fat droplets
What are LDLs?
Low Density Lipoprotein
ideally <100mg/dL
Still a necessary part of LIPID TRANSPORT
LDL-> peripheral tissue
Associated with Atherosclerosis = HARDENING of arteries
fat deposits in the lining of arteries –> CHD or artery blockage
What are HDL’s?
HIGH density Lipoprotein
ideally >40 mg/dL
Aids in the REMOVAL OF CHOLESTEROL
from arterial wall plaques
LDL -> Peripheral Tissue -> HDL -> back to LIVER
reduce risk of Atherosclerosis
What are S/Sx of High Serum Lipids?
And What CAUSES this?
- *XANTHOMAS** = swelling full of lipids
- *Enlarged LIVER / SPLEEN**
caused by:
high calorie diet / lack of exercise / cigarettes
T2DM / corticosteroids / estrogens / retinoids
B-adrenergic blocking agents
Optimal fasting serum levels:
Total cholesterol < 200 mg/dL
LDL cholesterol < 100 mg/dL
HDL cholesterol > 40 mg/dL
TG < 150 mg/dL
What are Routine Assay methods for
Cholesterol & Triglycerides?
Serum / Plasma Sample + enzymes
Measure H2O2 = hydrogen peroxide –> colored dye
measured SPECTROPHOTOMETRICALLY
similar for both Cholesterol / TG’s
What are Routine Assay methods for
HDL?
Precipitate HDL containing apo B-100
using cetrifugation and heparin-MnCl2
measure cholesterol REMAINING in the SUPERNATANT
(VLDL + LDL + chylomicrons)
What are Routine Assay methods for
LDL?
Selectively precipitate LDL, using polyvinyl sulfate or heparin
@ low pH, then measure cholesterol in supernatent
LDL = (Supernatent value) -MINUS- (TOTAL Cholesterol)
What are Routine Assay methods for
Total LipoProtein
NMR
to measure lipoprotein associated FA methyl groups
Electrophoresis
to seperate lipoproteins
What does Dehydration result in?
And what are the 3 types of Dehydration?
HYPER-Natremia + HYPER-Osmolarity
- *HYPER-Natremic** Dehydration
from: water & food deprivation / sweating / diuresis / diuretic -
Normo*Natremic Dehydration
from: vomiting & diarrhea -
HypoNatremic* Dehydration:
from: diuretic therapy / inefficient adrenocorticoids + renal disease
(Na+ is high extracellularly, Na out)
What CAUSES Overhydration?
What is the RESULT?
NOT caused by Excessive Water Intake (POLYDIPSIA)
typically caused by IMPAIRED RENAL FUNCTION
too much water is retained by the kidney
hypoNatremia***, ***hypo-osmality
What is EXCESS Sodium associated with?
Na Out
Too much dietary salt
CHF + Liver / Renal Disease
Pregnancy
HYPER-Aldosteronism
AAS / FES / Ion-Selective Electrode
What is Sodium depletion associated with?
Vomitting / Diarrhea
Sweating
- Renal** / *_hypo-aldosteronism_
- *DM**
BURNS
AAS / FES / Ion-Selective Electrode
what is HYPER-Kalemia associated with?
- *K**idney is the major organ for excretion
- *K - IN**, very steep gradient INSIDE
Kidney disease
Crush / Crash Injuries
Damaged Cells -> LEAK POTASSIUM
AAS / FES / Ion-Selective Electrode
Chloride Balance
CL intake is mainly through Diet
Excretin is mainly through URINE, little through FECES
HYPER / Hypo - Chloremia
is associated with SODIUM excess or depletion
exceptions can occur during _acidosis / alkalosis_
Color-agents + spectral changes / Ion-Selective Electrode
Typical Methods for Assaying
ELECTROLYTES
ION-SELECTIVE ELECTRODE
for Sodium / Potassium / Chloride
Sweat
How do we Sample / TEST for this electrolyte?
Sodium
Sample:
- *Serum / Plasma**
- *Urine / Feces / GI Fluids**
AAS = Atomic Absorption Spectrophotometry
FES = Flame Emission Spectrophotometry
Ion-Selective Electrode
may also monitor a enzyme or chromophore
How do we Sample / TEST for this electrolyte?
Potassium
K IN
Sample:
Serum / Plasma ( no RBCs that could release K+)
AAS = Atomic Absorption Spectrophotometry
FES = Flame Emission Spectrophotometry
Ion-Selective Electrode
How do we Sample / TEST for this electrolyte?
Chloride
Sample:
Urine / Plasma / Serum
Titration with color agents + monitor spectral changes
Ion-Selective Electrode
How do we test for CYSTRIC FIBROSIS?
SWEAT
Assay for:
Conductivity
CHLORIDE SPECIFIC ELECTRODE
ion-selective electrode
LIVER PATHOLOGIES
Problems with EXCRETION:
- *Bile Acids_ & _Jaundice**
- Xenobiotic Metabolis*m = DRUG Metabolism
Hepatic Synthetic Function Dysruption:
metabolism of Carbs / Fats / Protein
Cirrhosis / portal HYPER tention / Varices / Ascites
Coagulation Factors
GALLSTONES
What is CHOLESTASIS?
and how is it Diagnosed?
Bile is NOT flowing from the liver -> duodenom
due to:
gallstones / malignant growths
liver disease / drugs
ALKALINE PHOSPHATASE = ALP
What does Bilirubin / frationation Test diagnose?
Jaundice
Disorders of metabolism
Jaundice in the NEWBORN
What does AST / ALT test for?
Aspartate / Alanine Aminotransferase
AST = Sensitive test of Hepatocellular Disease
ALT = Sensitive + More Specific test of Hepatocellular Disease
What does Albumin test help Dianose?
Indicator of SEVERITY & CHRONICITY
of hepatic fxn / disease
What does Prothrombin Time test DIAGNOSE for?
Test for liver disease’s SEVERITY
Cholestasis
also is tested by ALP
What is the biochemical origin of BILIRUBIN?
How is it Excreted?
Heme Breakdown product
Conjugated with GLUCURONIC ACID –> excreted in the FECES
= Direct Bilirubin
Indirect bilirubin = unconjugated form
Urobilinogen = reduced form of bilirubin
occurs when liver’s metablic capacity is exceeded
detected by a color change rxn in urine
How do we Assay BILIRUBIN?
Direct Bilirubin Assay
react with diazotized sulfanilic acid w/ serum / plasma
measure color change
Urine Specimen:
dipstick impregnated w/ diazo reagent
also gives color change
Assay difference between
Conjugated / Unconjugated / Total
BILIRUBIN
Total Bilirubin
Seperate assay with alcohol to ACCELERATE RXN
Conjugated = Direct Bilirubin Assay
reacted with diazotized sulfanilic acid, measure color change
- UNconjugated = Indirect Bilirubin, *_much slower RXN_
- *Total - Direct = Indirect**
How do we assay for
Total Protein & Albumin?
Dye-Binding:
FAST & CHEAP, but less delicate
Biuret
chemical rxn -> color change, dependent on AMIDE bonds
Lowry
chemical rxn -> color change, dependend on Tyr + Trp Content
Direct photometric
Measure UV absorbance @ 200-225nm
not preffered due to interfering substances
What do BIURET / LOWRY assays test for?
TOTAL PROTEIN / ALBUMIN
Biuret = amide bonds, color change
Lowry = Tyr + Trp content, color change
What are assays for SPECIFIC Liver Proteins?
ex.
Complement Factors / Clotting Factors
AST / ALT / LDH enzymes
IMMUNOASSAYS
kits are cheap, and fast + specific
some cross-reactivity w/ isozymes
Electrophoretic Assays of SERUM samples
good for seperating / quantating isozymes
What are specific PATHOLOGIES of
Gastric / Pancreatic / Intestinal Function?
and what are
typical markers?
Tumors of GI / Pancreas
Ulcers / Pancreatitis
Cystic Fibrosis
variety maldigestion/malabsorption disorder
Hormones / Enzymes / Unabsorbed food compotents
markers
Typically assayed by IMMONOASSAYS
What are selected HORMONES / ENZYMES that are tested for
Gastric / Pancreatic / Intestinal Function?
And how are they
ASSAYED?
MOST HORMONES = Immunoassay
Gastrin / VIP / GIP
Pepsin/pepsinogen
Trypsin / Elastase / Chymotrypsin
synthetic substratess -> color change + IMMUNOASSAY
- *Amylase / Lipase**
- *coupled enzyme reactions** -> colored products -> spectrophotometrically + IMMUNOASSAY
What are KEY MARKERS in
Bone / Mineral Disorders?
And how are they caused?
INORGANICS
Ca / Mg / Phosphate
from THERAPY
- *Diuretics** -> lower Mg2+, RAISE Ca2+
- *Lithium** -> RAISE BOTH Mg + Ca
- *Vit D / A** -> RAISE Ca
**Hormones** = **vit D** + **ParaThyroid hormone** Enzymes = **alkaline phosphatase**
How do we Test / Assay for this inorganic marker for Bone/mineral disorders?
Phosphate
Use Serum or Heperinized Plasma,
EDTA/other anticoags interfere with assay
ammonium molybdate ->
UV-Vis Abosprtion
How do we Test / Assay for this inorganic marker for Bone/mineral disorders?
Calcium / Magnesium
Using chelating dyes -> colored complex
UV-Vis Absorption
AAS
Ion-Selective Electrodes
How do we Test / Assay for this hormone/enzyme for Bone/mineral disorders?
Vitamin D & Metabolites
column chromatography
HPLC / UV Absorption / Immunoassay
How do we Test / Assay for this hormone/enzyme for Bone/mineral disorders?
IMMUNOASSAYS
for all
calcitonin / PTH / collagen telepeptides / osteocalcin
How do we Test / Assay for this hormone/enzyme for Bone/mineral disorders?
Alkaline Phosphates
marker for BONE FORMATION
Immunoassay
or Complicated enzymatic Methods
What are typical markers for TUMORS?
and how are they tested for?
May express Aberrant Proteins or Excess “normal” proteins
Unusual carbs / polysaccherides
Mutated Genes
IMMUNOASSAYS
some use DNA sequence detection
mass spectrometry
