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BioMedChem M3 > 25/26 - Basic Clinical LABS > Flashcards

25/26 - Basic Clinical LABS Flashcards

1
Q

Why are Labs Ordered?

A

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

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2
Q

Typical Labs ordered in an ANNUAL CHECKUP

A

CBC

Lipid + Glucose Panel

Liver Fxn Panel

Blood tests for kidney fxn

Urinalysis

Thyroid / C-reactive Protein / HbA1C

Vitamin D / Homocysteine / PSA

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3
Q

CBC

Typical Lab ordered for Annual Checkup

A

Complete Blood Count

includes:
WBC / RBC

WBC differential

Hematocrit / Hemogloblin

Platelet Count

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4
Q

Lipid + Glucose Panel

Typical Lab ordered for Annual Checkup

A

Total Cholesterol

LDL + HDL
LDL/HDL Ratio

Glucose

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5
Q

Liver (Hepatic) Function Panel

Typical Lab ordered for Annual Checkup

A

blood levels of:

Total Protein

Albumin / Bilirubin

Liver Enzymes

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6
Q

Blood tests for KIDNEY FUNCTION

Typical Lab ordered for Annual Checkup

A

Serum CREATININE

  • *BUN**
  • *blood urea nitrogen**
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7
Q

Urinalysis

Typical Lab ordered for Annual Checkup

A

Examine specimen for:
color / clarity / odor / pH / spgr

protein / glucose / ketones

Also microscopic analysis for:

bacteria / crystals / blood cells

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8
Q

Assays for VITAMIN status Focus on:

A

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

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9
Q

Vitamin A

How is it clinically assayed?

A

Fat Soluble

Vision / growth / Reproduction
night blindness

Fluorometric

HPLC / RIA

Photometric

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10
Q

Fat Soluble Vitamins

How are they clinically assayed?

A

(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

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11
Q

Vitamin D

How is it clinically assayed?

A

Fat soluble vitamin

Ca2+ metabolism / bones / teeth
rickets / osteomalacia

Competitive Binding Protein = CPB

HPLC / RIA

no photometric assay

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12
Q

Vitamin E

How is it clinically assayed?

A

Fat-soluble Vitamin

Antioxidant for unsat-lipids
lipid peroxidation / fragile RBC

Erythrocyte Hemolysis

HPLC, NOT RIA

Photometric

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13
Q

Vitamin K

How is it clinically assayed?

A

Fat-Soluble Vitamin

blood clotting / osteocalcins
increased clotting time + hemorrhages

ProThrombin Time

HPLC / RIA

Photometric

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14
Q

Thiamine

Water Soluble Vitamin, how is it CLINICALLY ASSAYED?

A
  • *B1**
  • beri beri*

HPLC / Fluorometric / microbial

Transketolase

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15
Q

Riboflavin

Water Soluble Vitamin, how is it CLINICALLY ASSAYED?

A

B2
redox / dermatitis, photophobia

Enzyme

HPLC / Fluorometric / Microbial

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16
Q

Pyridoxine

Water Soluble Vitamin, how is it CLINICALLY ASSAYED?

A

B6
AA + phospholipid metabolism / anemia + convulsions

Tyrosine Decarboxylase

HPLC / no fluoro / Microbial

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17
Q

Niacin

Water Soluble Vitamin, how is it CLINICALLY ASSAYED?

A

B3
REDOX / pellagra

Fluorometric / Microbial

no HPLC, too common in the immune system

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18
Q

Folate

Water Soluble Vitamin, how is it CLINICALLY ASSAYED?

A

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

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19
Q

Cyanobalamin

Water Soluble Vitamin, how is it CLINICALLY ASSAYED?

A

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*
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20
Q

Biotin

Water Soluble Vitamin, how is it CLINICALLY ASSAYED?

A

B7
Carboxylation / dermatitis

AVIDIN BINDING

Enzymes

PHOTOmetric

Microbial

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21
Q

Pantothenic Acid

Water Soluble Vitamin, how is it CLINICALLY ASSAYED?

A

B5
Central metabolism / burning feet syndrome

Enzymes

CPB

PHOTOmetric

Microbial

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22
Q

Ascorbate

Water Soluble Vitamin, how is it CLINICALLY ASSAYED?

A

C
connective tissue / scurvy

PHOTOmetric

HPLC

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23
Q

What Vitamin can be analyzed by

Erythrocyte Hemolysis?

A

Vitamin E

antioxidant / lipid peroxidation

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24
Q

Which Vitamin can be analyzed by

PROTHROMBIN TIME?

A

Vitamin K

blood clotting / hemorrhages

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25
Q

Which vitamins can be analyzed by

IMMUNOASSAY?

A

FOLATE + Cyanobalamin
B9 / B12

both also CPB & Microbial assays

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26
Q

Which vitamin can be analyzed by

AVIDIN BINDING?

A

BIOTIN

B7

carboxylation / dermatitis

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27
Q

Oral Glucose Tolerance Test

What is done prior / during the test?

A

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

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28
Q

Oral Glucose Tolerance Test

What does it measure?

What is a normal response?

A

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

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29
Q

OGTT

What is a Diabetic/abnormal Response?

What values indicates Diabetes?

A

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
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30
Q

Main differences in clinical test results for

Diabetic vs Non-diabetic

A
  • *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)

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31
Q

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.

A

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**
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32
Q

What is often shown in PREDIABETES?

A
  • *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

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33
Q

3 Ways to DIAGNOSE DM by blood glucose levels

What levels?

A

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

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34
Q

What are the 3 Ketone Bodies?

involved in KETOSIS

A

Acetone

B-hydroxybutyrate

Acetoacetate

Organic acids, if their levels rise TOO HIGH –> blood pH = ACIDIC

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35
Q

At what LEVELS is KETOSIS seen?

What symptoms are seen?

A

Seen with levels of 30-70 mmol/L

Acetone on the breath may be detectible

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36
Q

When does Acidotic Ketosis occur?

A

when the Blood pH DROPS BELOW 7.3

B-hydroxbutyrate + acetoacetate
Organic acid, concentrations are TOO HIGH
overcome the buffering action of the serum

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37
Q

What are the 2 TYPES of

BLOOD GLUCOSE METERS?

and what do they measure?

A

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

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38
Q

What does HbA1c measure?

And how is it correlated with Diabetes?

A

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

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39
Q

What is NITROGEN BALANCE?

24-hour urine collection used to measure

What are its Positive / Negative values?

A

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*
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40
Q

Where are AA’s filtered out from?

What occurs if the transport is saturated or defective?

A

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

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41
Q

What causes PRIMARY Acidurias?

A

MUTATIONS IN ENZYMES
that are involved in AA metabolism

loss in activity of enzyme –> RAISES concentration of precursors
which will appear in the urine

42
Q

What is SECONDARY Aciduria?

A

DAMAGE TO KIDNEY
from various causes:

Viral infection / APAP toxicity / Rickets

Genetic defects in enzyme/transporters in kidney

43
Q

What are SCREENING TESTS for

Aminoacidurias?

A

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

44
Q

What are QUANTITATIVE TESTS

for AminoAcidurias?

A

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

45
Q

OTHER Organic ACIDURIAS

other secondary metabolites

A

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
46
Q

What type of Analysis/Test is done for

VOLATILE ANYLYTES?

A

GC / MC

for small volatile analytes = you can SMELL IT
Ex. Maple Syrup - MSUD

NOT used for amino Acids

47
Q

What are anlytes for KIDNEY FUNCTION TESTS?

Where do the specimens come from?

A

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

48
Q

What levels/tests are used to monitor the

filtration ability of the KIDNEY?

A

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

49
Q

What ORGAN(S) do UREA LEVELS track the health of?

A

BOTH

LIVER + KIDNEY

Synthesis is in the liver
Excretion is through the kidney

Urea is the MAJOR route by which we excrete NITROGEN

50
Q

How do we clinically ASSAY

UREA?

A

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

51
Q

What are physiological sources of

AMMONIA?

A

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*
52
Q

HYPER-Ammonemia

Causes / Effects

A

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

53
Q

How is Ammonia Analyzed / tested for?

A

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

54
Q

Creatine vs CreaTINine

A

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

55
Q

What does CreaTINine clearance reflect?

What organ?

CrCl

A

Reflects the ability of the KIDNEY to

FILTER metabolic byproducts from the BLOOD

56
Q

How is Creatine / CreaTINine Analyzed/Assayed?

A

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

57
Q

How is Uric Acid (Urate) produced?
what does it do?

A
  • *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.

58
Q

What is HYPER-Uricemia?

What diseases does it cause?

A

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

59
Q

How is Urate/Uric Acid Clinically ASSAYED?

A

HPLC

Phosphotungstic Acid = PTA
BLUE color as PTA is reduced by urate

Uricase
UV absorbance as enzyme, urea -> allotoin

Dry chemistry systems

60
Q

Sketch the transport of LIPIDS

throughout the BODY

A
61
Q

What is the role of Lipoproteins?

A

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

62
Q

What are LDLs?

A

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

63
Q

What are HDL’s?

A

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

64
Q

What are S/Sx of High Serum Lipids?

And What CAUSES this?

A
  • *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

65
Q

What are Routine Assay methods for

Cholesterol & Triglycerides?

A

Serum / Plasma Sample + enzymes
Measure H2O2 = hydrogen peroxide –> colored dye

measured SPECTROPHOTOMETRICALLY

similar for both Cholesterol / TG’s

66
Q

What are Routine Assay methods for

HDL?

A

Precipitate HDL containing apo B-100

using cetrifugation and heparin-MnCl2

measure cholesterol REMAINING in the SUPERNATANT

(VLDL + LDL + chylomicrons)

67
Q

What are Routine Assay methods for

LDL?

A

Selectively precipitate LDL, using polyvinyl sulfate or heparin
@ low pH, then measure cholesterol in supernatent

LDL = (Supernatent value) -MINUS- (TOTAL Cholesterol)

68
Q

What are Routine Assay methods for

Total LipoProtein

A

NMR
to measure lipoprotein associated FA methyl groups

Electrophoresis
to seperate lipoproteins

69
Q

What does Dehydration result in?

And what are the 3 types of Dehydration?

A

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)

70
Q

What CAUSES Overhydration?

What is the RESULT?

A

NOT caused by Excessive Water Intake (POLYDIPSIA)

typically caused by IMPAIRED RENAL FUNCTION
too much water is retained by the kidney

hypoNatremia***, ***hypo-osmality

71
Q

What is EXCESS Sodium associated with?

Na Out

A

Too much dietary salt

CHF + Liver / Renal Disease

Pregnancy

HYPER-Aldosteronism

AAS / FES / Ion-Selective Electrode

72
Q

What is Sodium depletion associated with?

A

Vomitting / Diarrhea

Sweating

  • Renal** / *_hypo-aldosteronism_
  • *DM**

BURNS

AAS / FES / Ion-Selective Electrode​

73
Q

what is HYPER-Kalemia associated with?

A
  • *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

74
Q

Chloride Balance

A

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

75
Q

Typical Methods for Assaying

ELECTROLYTES

A

ION-SELECTIVE ELECTRODE

for Sodium / Potassium / Chloride

Sweat

76
Q

How do we Sample / TEST for this electrolyte?

Sodium

A

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

77
Q

How do we Sample / TEST for this electrolyte?

Potassium

K IN

A

Sample:
Serum / Plasma ( no RBCs that could release K+)

AAS = Atomic Absorption Spectrophotometry

FES = Flame Emission Spectrophotometry

Ion-Selective Electrode

78
Q

How do we Sample / TEST for this electrolyte?

Chloride

A

Sample:
Urine / Plasma / Serum

Titration with color agents + monitor spectral changes

Ion-Selective Electrode

79
Q

How do we test for CYSTRIC FIBROSIS?

A

SWEAT

Assay for:
Conductivity

CHLORIDE SPECIFIC ELECTRODE
ion-selective electrode

80
Q

LIVER PATHOLOGIES

A

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

81
Q

What is CHOLESTASIS?

and how is it Diagnosed?

A

Bile is NOT flowing from the liver -> duodenom

due to:
gallstones / malignant growths
liver disease / drugs

ALKALINE PHOSPHATASE = ALP

82
Q

What does Bilirubin / frationation Test diagnose?

A

Jaundice

Disorders of metabolism

Jaundice in the NEWBORN

83
Q

What does AST / ALT test for?

Aspartate / Alanine Aminotransferase

A

AST = Sensitive test of Hepatocellular Disease

ALT = Sensitive + More Specific test of Hepatocellular Disease

84
Q

What does Albumin test help Dianose?

A

Indicator of SEVERITY & CHRONICITY

of hepatic fxn / disease

85
Q

What does Prothrombin Time test DIAGNOSE for?

A

Test for liver disease’s SEVERITY

Cholestasis
also is tested by ALP

86
Q

What is the biochemical origin of BILIRUBIN?

How is it Excreted?

A

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

87
Q

How do we Assay BILIRUBIN?

A

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

88
Q

Assay difference between
Conjugated / Unconjugated / Total
BILIRUBIN

A

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**
89
Q

How do we assay for

Total Protein & Albumin?

A

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

90
Q

What do BIURET / LOWRY assays test for?

A

TOTAL PROTEIN / ALBUMIN

Biuret = amide bonds, color change

Lowry = Tyr + Trp content, color change

91
Q

What are assays for SPECIFIC Liver Proteins?
ex.
Complement Factors / Clotting Factors

AST / ALT / LDH enzymes

A

IMMUNOASSAYS
kits are cheap, and fast + specific
some cross-reactivity w/ isozymes

Electrophoretic Assays of SERUM samples
good for seperating / quantating isozymes

92
Q

What are specific PATHOLOGIES of

Gastric / Pancreatic / Intestinal Function?

and what are
typical markers?

A

Tumors of GI / Pancreas

Ulcers / Pancreatitis

Cystic Fibrosis

variety maldigestion/malabsorption disorder

Hormones / Enzymes / Unabsorbed food compotents
markers

Typically assayed by IMMONOASSAYS

93
Q

What are selected HORMONES / ENZYMES that are tested for

Gastric / Pancreatic / Intestinal Function?​

And how are they

ASSAYED?

A

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
94
Q

What are KEY MARKERS in

Bone / Mineral Disorders?

And how are they caused?

A

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**
95
Q

How do we Test / Assay for this inorganic marker for Bone/mineral disorders?

Phosphate

A

Use Serum or Heperinized Plasma,
EDTA/other anticoags interfere with assay

ammonium molybdate ->

UV-Vis Abosprtion

96
Q

How do we Test / Assay for this inorganic marker for Bone/mineral disorders?

Calcium / Magnesium

A

Using chelating dyes -> colored complex

UV-Vis Absorption

AAS

Ion-Selective Electrodes

97
Q

How do we Test / Assay for this hormone/enzyme for Bone/mineral disorders?

Vitamin D & Metabolites

A

column chromatography

HPLC / UV Absorption / Immunoassay

98
Q

How do we Test / Assay for this hormone/enzyme for Bone/mineral disorders?

A

IMMUNOASSAYS

for all

calcitonin / PTH / collagen telepeptides / osteocalcin

99
Q

How do we Test / Assay for this hormone/enzyme for Bone/mineral disorders?

Alkaline Phosphates

A

marker for BONE FORMATION

Immunoassay

or Complicated enzymatic Methods

100
Q

What are typical markers for TUMORS?

and how are they tested for?

A

May express Aberrant Proteins or Excess “normal” proteins

Unusual carbs / polysaccherides
Mutated Genes

IMMUNOASSAYS

some use DNA sequence detection

mass spectrometry

BioMedChem M3 (8 decks)

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