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Clinical Chemistry II - 4378 > Blakes Clinical Chemistry lab Study questions > Flashcards

Blakes Clinical Chemistry lab Study questions Flashcards

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1
Q

Gold standard of glucose methodology

A

hexokinase method
- due to its higher specificity
- its a coupled enzyme assay uses hexokinase enzyme to convert NADP to NADPH

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2
Q

Hexokinase method reaction

A

1.) glucose + ATP by enzyme hexose kinase —> glucose-6-phosphate + ADP
2.) glucose-6-phosphate (enzyme G-6-PD)—> 6-phosphogluconate (NADP—>NADPH)

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3
Q

Glucose can be measured in the

A

Blood, serum, plasma, urine, and body fluids

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4
Q

When glucose is measured in whole blood the values are

A

10-12% less then serum

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5
Q

Glucose testing
separate cells from

5-7% what

A

serum and or plasma within 1 hour to prevent the loss of glucose through glycolysis ( decreases 5-7%/hour)

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6
Q

Glucose testing
acceptable draw tubes

A

Red, gold, and green, and gray

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7
Q

Glucose oxidase method

A

coupled enzyme assay using the glucose oxidase enzyme
this is cheaper then 2 methodologies

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8
Q

Glucose oxidase reaction

A

Glucose reacts with water and Oxygen with glucose oxidase and makes glyconic acid and H202. then H202 uses peroxidase to produce a color change which is directly proportional to the glucose concentration in the sample

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9
Q

Glucose oxidase reaction

High levels of what contribute to decreased readings

A

high levels or bilirubin, uric acid, and ascorbic acid all contribute to decreased readings

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10
Q

Oral glucose tolerance test

The patient must be

A

Fasting

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11
Q

Oral glucose tolerance testing

Fasting samples are drawn and the patient

A

drinks 100 grams of glucose and then samples are drawn at 30 minutes, 1 hour, 2 hours, and 3 hours after the drink is consumed.

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12
Q

Oral glucose tolerance testing

not recommended by the

A

ADA to diagnosis diabetes, but its commonly used to screen for gestational diabetes

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13
Q

Oral glucose tolerance testing

sometimes a 2 hour

A

Postprandial challenge is performed instead, where you use 75 grams of glucose, and then one sample is drawn 2 hours after the drink is consumed

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14
Q

Glycosylated hemoglobin

A

A1c

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15
Q

glycosylated hemoglobin A1c

long-

A

Long term blood glucose regulation followed by measurements of glycosylated hemoglobin

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16
Q

glycosylated hemoglobin A1c

A good way to monitor how a

A

A Diabetic patient managed their sugar levels over the long haul

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17
Q

glycosylated hemoglobin A1c

Essentially the glucose sticks

A

to the hemoglobin

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18
Q

glycosylated hemoglobin A1c

The reaction does not

A

Require a enzyme

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19
Q

glycosylated hemoglobin A1c

Gold standard for measurement

A

HPLC

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20
Q

glycosylated hemoglobin A1c

If a patient has a condition effecting blank shouldn’t be monitored this way

A

RBC survival shouldn’t be monitored this way

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21
Q

glycosylated hemoglobin A1c

Reference range

A

4.0-6.5%

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22
Q

Other tests include of glucose testing

A

ketone testing

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23
Q

Ketone testing

produced by the

A

liver through the metabolism of FAs

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24
Q

Ketones provides

A

ready energy source from stored lipids

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25
Q

Ketones increase

A

with carbs deprivation, or decreased carbohydrates use ( diabetes, dehydration, starvation, and high fat diets)

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26
Q

3 ketone bodies

A

Acetone, acetoacetic acid, and BHOB

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27
Q

Ketones measured in

A

urine and serum/plasma

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28
Q

Triglyceride functions

Major form of what

Primary function

The human body stores large amounts of blank and this form for reserve energy is

A

-Major form of fat found in nature
-Primary function is to provide energy for the cell
-The human body stores large amounts of fatty acids in ester linkages with glycerol in the adipose tissue. This form of reserve energy storage is highly efficient because of the magnitude of the energy released when fatty acids undergo

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29
Q

Triglyceride clinical significance

A

-Triglyceride testing is used to understand your risk for heart disease, stroke, and other conditions that involve your arteries, such as PAD (Peripheral Arterial disease)
-Also used to help monitor heart conditions and treatments to lower the risk of heart disease

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30
Q

Triglyceride adult levels

A

adults<150mg/dl

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31
Q

TG kids and teens level

A

kids<90mg/dl

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32
Q

Borderline TG level

A

150-190mg/dl

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33
Q

High TG level

A

200-499mg/dl

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34
Q

Extremely high TG level

A

> 500mg/dL

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35
Q

What causes elevated Triglyceride values

A

-Drinking too much alcohol
-Eating too many refined carbohydrates (white breads), sugars, or saturated fat combined w/ a sedentary lifestyle
-Genetics
-Certain medical conditions like diabetes, hypothyroidism, Lupus, Liver or Kidney disease, RA, or obesity
-Medications (2nd gen. Antipsychotics I.e. clozapine, Antiretrovirals, Corticosteroids, Beta blockers, etc.)

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36
Q

Triglyceride possible treatment options

A

-Lifestyle Changes
-Avoid alcohol, refined carbs and sugars
-Eat more seafood that contain omega- 3 fatty acids.
Exercise more often lose weight

-Medications: Fibrates or Statins

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37
Q

Chemistry assays that can be affected by extreme lipemia

A

-In cases of Extreme Lipemia, the following testing cannot be reported (UNLESS IT CAN BE REMOVED OR DILUTED)
Albumin
Total Bilirubin
Cortisol
HDL
Lactic Acid
Phosphorus
Vitamin D 25-OH

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38
Q

Triglyceride

How do you remove them from your sample

A

-Diltuions
-High Speed Centrifugation: 10000 xg for 15 minutes
-Ultracentrifuge: Higher speed centrifuge which effectively separates the larger molecules like lipids from the patient serum or plasma
-Chloroform: YES SERIOUSLY….BUT FOR OBVIOUS REASONS WE DON’T USE THIS IN THE CLINICAL SETTING
-Lipoclear: a polar solvent that can be used to separate lipids from the aqueous in lipemia samples (you just mix it with your sample and spin), but it can interfere with other tests such as GGT, CRP, and CK

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39
Q

Cholesterol biological function

A

-Structural component of cell membranes
-Serves as a building block for synthesizing various steroid hormones and Vitamin D, and bile acids

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40
Q

Cholesterol clinical significance

A

Total cholesterol is measured in a clinical setting to help determine your risk of developing heart disease. It can determine your risk of the build up of fatty deposits (plaques) in your arteries that can lead to narrowed or blocked arteries throughout your body (atherosclerosis). If one of the plaques burst, a blood clot may form that may block the artery completely or travel to other parts of the body causing heart attack, stroke vascular dementia, or limb los

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41
Q

Cholesterol normal range

A

less then 200mg/dl

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42
Q

Cholesterol borderline to elevated

A

200-239mg/dl

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43
Q

high cholesterol value

A

above 240mg/dl

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44
Q

high cholesterol value

A

above 240mg/dl

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45
Q

Cholesterol elevation causes

A

Poor diet Eating too much-saturated fat or trans fat
Obesity
Lack of Exercise
Smoking
Alcohol
Age

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46
Q

Cholesterol
ways to reduce cholesterol

A

-Heart healthy eating Limiting trans and saturated fats
-Weight Management
-Increase Physical Activity
-Managing Stress
-Quit Smoking
-Reduce Alcohol Intake

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47
Q

Triglyceride and cholesterol AMR and CRR

A

-AMR: (Linearity ) Analytical Measurable Range of your chemistry analyzer (or the methodology of the reagent it uses)
-Clinical Reportable Range: Results outside the CRR will be reported as a less than or greater than. Dilutions performed by the chemistry analyzers are performed using Saline
Triglyceride
AMR 7-1400 mg/dL
Max Dilution 1:4
CRR 7-5600 mg/dL

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48
Q

Triglyceride and Cholesterol AMR and CRP continued

Cholesterol AMR and CRP

A

Total Cholesterol
-AMR 5-700 mg/dL
-Max Dilution 1:4
-CRR 5-2800 mg/d

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49
Q

Triglyceride and cholesterol acceptable specimen types and stability

A

-The preferred specimen type in the clinical laboratory setting is Lithium Heparinized Plasma or Serum.
-Triglycerides: 2 days RT, 7 days refrigerated, 1 year frozen
-Cholesterol: 7 days RT, 7 days refrigerated, 3 months frozen

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50
Q

Marked elevations of AST and ALT are associated with

A

Marked elevations of AST and ALT are associated with hepatocellular disease or damage to hepatocytes

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51
Q

Marked elevation of ALP is associated with

A

Marked elevation of ALP is associated with hepatobiliary disease or obstructive liver disease.

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52
Q

Hepatocellular diseases

A

liver cancer, cirrhosis

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53
Q

Hepatobiliary diseases

A

: a group of conditions affecting the bile duct, pancreas, and gallbladder

54
Q

AST can also be elevated in

A

myocardial diseases such as Congestive heart failure, pericarditis, and myocardial infarctions

55
Q

Viral hep, cirrhosis, alcoholic hep and reyes syndrome are examples of

A

AST elevations.

56
Q

second most common cause of AST elevation

A

Steatohepatitis

57
Q

Muscle diseases associated with AST elevations are

A

Muscular dystrophy and skeletal muscle injury.

58
Q

ALT is more

What is hugest elevations

A

Specific then AST and acute viral hep and toxic hep is highest elevations

59
Q

ALT is more

A

Specific then AST and acute viral hep and toxic hep is highest elevations

60
Q

AST and ALT can be elevated before

A

Liver cancer

61
Q

AST is routinely measured using a modification of the

blank is the Indicator reaction

and measured ABS as a decrease in blank

A

Karmen method with the addition of coenzyme P-5-P to ensure full catalytic activity

Malate dehydrogenase is the indicator reaction the measures the decrease in absorbance at 340 nm as NADH is oxidized to NAD+, which is directly proportional to the AST activity

62
Q

AST methodology

A

1.) L-aspartate + a-ketoglutarate with enzymes Asoatate aminotransferase and P-5-P <——-> Oxaloacetate + L-glutamate

2.) Oxaloacetate + NADH + H+ with enzyme Malate dehydrogenase ——> Maltate + NAD+

63
Q

ALT methodology

A

ALT is routinely measure with a modification of Wroblewski and LaDue using lactate dehydrogenase as the indicator reaction
The decrease in an absorbance is measured at 340 nm as NADH is oxidized to NAD+

64
Q

ALT reaction

A

1.)Alanine + a-ketoglutarate with enyzme Alanine aminotransferase and P-5-P —–> Pyruvate + L-Glutamate

2.) pyruvate + NADH with enzyme Lactate dehydrogenase ——-> L-Lactate + NAD+

65
Q

AST and ALT reference range

A

AST: 37C is 5-30 U/L

ALT: 37C is 6-37 U/L

66
Q

Hemolysis should be avoided in AST because AST

A

is 10-15 times higher in RBCs than in serum

67
Q

Hemolysis should be avoided because ALT levels

A

In RBCs are 5-8 times higher than serum levels

68
Q

AST is stable at room temperature for

A

48 hours and 3-4 days at refrigerator temperature

69
Q

ALT should be measured witin

A

24 hours because activity decreases in refrigerated temperatures but is stable when frozen at -70 degrees C

70
Q

CRP is what

A

Clinical reportable range

71
Q

AMR is

A

Analytical measurable range

72
Q

AST: CRP=

A

AMR because it has no validated dilution

73
Q

ALT: CRP requires a

A

1:5 dilution

All to report

The highest to report is the high end of the clinical range.

74
Q

Enyzmes sometimes have

A

Absorbance errors

75
Q

Using cellulose acetate, serum proteins can be

A

separated into 6 fractions

76
Q

six fractions of serum protiens

A

Albumin with higest peak, then Alpha1, alpha 2, Beta, and gamma

77
Q

Beta can be subdivided into

A

Beta 1 and Beta 2

78
Q

Albumin range range

A

3.2-5.0 g/dL

79
Q

Alpha 1 globulins range

A

0.1-0.4 g/dL

80
Q

Alpha 2 globulins range

A

0.6-1.0 g/dL

81
Q

Beta globulins range

A

0.6-1.3g/dL

82
Q

Gamma globulins range

A

0.7-1.5 g/dL

83
Q

Albumins low molecular weight confers that

A

It migrates most Anodally

84
Q

Albumin forms complexes with

A

Many proteins and permitting transport of calcium and Billary pigments.

85
Q

Albumin plays a role in

A

Maintaining blood volume and osmotic pressure

86
Q

gamma globulins are also called

A

Immunoglobulins IgM

87
Q

Globulins are very

A

Heterogeneous

88
Q

Albumin is very

A

Homogeneous

89
Q

The rapid breakdown of tissue is frequently found in

A

Acute inflammation and is characterized by localized biochemical responses such as activation of complement and by cellular responses such as mobilization of phagocytes and increased in protein synthesis.

90
Q

Acute inflammation picture

A
91
Q

Subacute Inflammation

A

represents a intermediate stage between two possible courses of inflammation which as total convalescence or recovery and the second being Chromic inflammatory condition

when recovery begins there is a characteristic decrease followed by return to normal of the Alpha 1 globulins, complement, and albumin

92
Q

Chronic inflammation

A

Increase in proteins called Chronic phase proteins.

Electrophoretically this is seen as a moderate to slight increase in alpha 2 globulins and a slight increase in the beta globulins

93
Q

Chronic inflammation

Albumin may be

A

Slightly suppressed with a polyclonal increase in gamma globulin

94
Q

Chronic inflammation picture

A
95
Q

Liver is the site of

A

Albumin and Alpha globulin synthesis

96
Q

The liver has significantly what

A

reserve synthesis capacity

97
Q

Decreased Albumin is only seen in

A

Advanced hepatocellular diseases

98
Q

Acute viral hepatitis

A

Increased levels of IgG and IgM

99
Q

Chronic liver disease

A

marked increase in IgG,M,A with a decrease in albumin and transferrin

100
Q

Biliary destruction

A

increased levels of C4 and beta lipopotien

101
Q

Liver disease picture

A
102
Q

Nephrotic syndrome

involves a large loss

A

involves a large loss of Albumin from the kidneys

103
Q

nephortic syndrome can be caused by

A

Diabetes Mellitus, Connective tissue disease, glomerular disease, and circulatory diseases.

104
Q

Nephrotic syndrome is characterized by

A

Hypoproteinemia
edema
Hyperlipedemia
Proteinuria

105
Q

Albumin and other low molecular weight proteins are lost through the glomerular tubules in

A

Nephrotic syndrome therefore there is a increase in large molecular weight proteins ( IgM, macroglobulin, and Lipoproteins)

106
Q

Nephrotic syndrome

The electrophoresis pattern may be

A

Mimicked by acute inflammatory conditions when increased alpha 1 and 2 globulins

107
Q

Nephrotic syn picture

A
108
Q

Hypogammaglobulinemia and Agammaglobulinemia

are characterized by

A

decreased amount of all immunoglobulins.

109
Q

Hypogammaglobulinemia and Agammaglobulinemia

examples in infants

A

Wiskott aldrich syndrome, Brutons disease, ataxia telangietasia

110
Q

Hypogammaglobulinemia and Agammaglobulinemia

accuquired in childhood

A

monoclonal gammopathies, or induced by immunosuppressive therapy

111
Q

Bence jones proteins

A

are found in adults with hypogammaglobulinemia

112
Q

Monoclonal gammopathies

A

proliferation of B lymphocytes

electrophoresis shows one homogeneous peak

decreased in normal immunoglobulins

113
Q

Homogenous paraproteins are formed from a single type of heavy chain that filters through the glomerular tubules and forms

A

Bence jones proteins( free light chains

114
Q

Electrophoresis is not suitable for

A

Biclonal gammopathies Immunoelectrophoresis or Immunofixation must be performed.

115
Q

Immunofixation electrophoresis consists of

A

Agarose gel electrophoresis followed by immunoprecipitation by direct application of specific antisera

116
Q

Polycolonal gammopathies are characterised by

A

Broad, diffuse increase in the gamma region of IgG, A, M.

After hypoalbyminemia, polyclonal gammopathy is the most common protein abnormality

117
Q

Polyclonal gammopathies are seen in

A

Chronic liver disease
Collagen disorders
Chronic infections
metastatic carcinoma
cystic fibrosis
thermal burns during recovery stage

118
Q

In heterozygous individual alpha one antitrypsin is decreased

A

30-50%

119
Q

Homozygous individual alpha one antitrypsin deficiency

A

can decrease as much as 80-90%

Homozygous individual are exposed to pulmonary emphysema

120
Q

Acquired alpha one antitrypsin deficiencies

A

Nephrotic syndrome

Phenotyping done by 2-dimensional immunoelectrophoresis is done or by isoelectrofocusing in polyacrylamide gel

121
Q

A super-high serum sodium low ca2+ and Mg2+ usually indicative of low

A

accidentally placing specimen into wrong tube. or nurse dumps tube into another one.

potassium chelates Mg2+ and Ca2+

122
Q

Hemolysis is the most encountered

A

Artifact in the lab, can be as high as 3.3% of all routine samples , thus accounting for 40-70% of all unsuitable samples identified.

123
Q

Rejection of in vivo hemolysis is considered

A

Malpractice

124
Q

In vivo

A

Inside the body

125
Q

In vitro

A

Outside the body

126
Q

Icteric is

A

Jaundice= yellowish color of the eyes

very high bilirubin concentrations

127
Q

A dextrose solution (sugar) IV infusion would yield

A

extremely high glucose results results in venous specimens

Collected above or near the Infusion site

128
Q

Total parenteral nutrition (TPN) fluid contains most

A

of the required daily nutrients for a person who cant ingest food

TPN fluid contamination in a specimen creates gross turbidity along with elevated lipid and glucose values and potassium levels too high to be compatible with life (< l.3 and > 9 mmol/l “ RI 3.5-5.0mmol/L).

Have to turn off TP< machine first before chemistry lab testing

129
Q

In specimens from a patient receiving a saline IV infusion

A

Sodium and chloride results will be falsely elevated due to contamination from saline IV fluid.

130
Q

Lipemic plasma

A

will appear milky white

the most common cause of lipemic samples Is that the patient has not fasted.

131
Q

Hemolysis impacts lab testing because

A

Increase in intracellular analytes such as Aspartate aminotransferase, Lactate dehydrogenase, and Potassium.

released proteases from RBCs can degrade proteins such as insulin and cardiac troponin.

The presence of hemoglobin can interfere with spectrophotometric readings

132
Q

Lipemic samples interfere with

A

increase light abs and decrease light Transmittance.

can cause volume discrepancies

severe lipemic samples are more prone to hemolysis.

Clinical Chemistry II - 4378 (28 decks)

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