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Clinical Chemistry > Blood Analytes > Flashcards

Blood Analytes Flashcards

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1
Q

Major source of energy in the body

A

Glucose

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2
Q

Chemical structure of glucose

A

mono, di and polysaccharides

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3
Q

Glucose Metabolism?

A
  • Glycolysis, Glycogenesis, etc.
  • Enzymes
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4
Q

Regulates glucose by increasing cellular uptake and promoting glycogenesis

A

Insulin

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5
Q

Regulates glucose by stimulating glycogenolysis and gluconeogenesis

A

Glucagon

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6
Q

Regulates glucose by elevating glucose levels

A

Epinephrine

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7
Q

Function to elevate glucose levels

A

GH, ACTH, Cortisol, and Thyroid hormones

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8
Q

Person has this when fasting blood sugars are greater than or equal to 120 mg/dL

A

Hyperglycemia

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9
Q

Causes of Hyperglycemia

A

Diabetes mellitus (type 1, 2, and gestational)
Liver Failure

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10
Q

Symptoms of Hyperglycemia

A
  • Glucosuria
  • nausea/vomiting
  • malaise
  • diarrhea
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11
Q

Person has this when fasting blood sugars are less than or equal to 50 mg/dL

A

Hypoglycemia

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12
Q

Causes of Hypoglycemia

A
  • hormone deficiency
  • drug reaction
  • insulin excess
  • genetic disorder
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13
Q

Symptoms of Hypoglycemia

A
  • nausea
  • trembling/sweating
  • rapid pulse
  • lightheadedness
  • watch CNS symptoms
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14
Q

Diabetes mellitus type 1 (insulin dependent)

A

Caused by autoimmune destruction of pancreatic beta cells, juvenile onset
- hyperglycemia
- ketosis

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15
Q

Diabetes mellitus Type 2 (non-insulin dependent

A

Caused by insulin resistance and insulin deficiency
- obesity

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16
Q

Lab tests for blood glucose

A

Direct measurement
Urine
Glucose tolerance test (GTT)
- evaluates insulin response challenge
Glycosalated Hgb (Hgb A1c)

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17
Q

nitrogen-containing metabolite of protein catabolism

A

Urea

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18
Q

Blood urea nitrogen is synthesized in ____ (CO2 + NH3) and excreted in kidney

A

Liver

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19
Q

Urea (BUN) is dependent on

A

exogenous nitrogen intake and endogenous protein catabolism

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20
Q

Disorder of elevated urea

A

Azotemia

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21
Q

Causes of prerenal azotemia

A
  • decreased renal blood flow; CHF,
    shock, dehydration
  • increased protein breakdown
  • high protein diet
  • GI hemorrhage
  • Obstruction
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22
Q

Azotemia brought on by renal failure

A

Renal azotemia

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23
Q

toxic condition; high serum urea accompanied w/renal failure

A

Uremia

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24
Q

Causes of Decreased BUN

A
  • Liver failure
    -Overhydration (SIADH)
    -Negative nitrogen balance (protein depletion)
    -Pregnancy
    -Nephrotic syndrome
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25
Q

Creatinine levels in the blood

A

Relative to muscle mass and body weight
Low variance
Primarily measured for Glomerular Filtration Rate (GFR), # of functioning nephrons
Associated with BUN

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26
Q

BUN/Creatinine ratio

A

12-20 mg urea/mg creatinine.
Helps determine cause of azotemia
Both BUN & Creatinine elevated indicate post renal obstruction or prerenal azotemia superimposed on kidney disease

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27
Q

High BUN/Creatinine ratio

A

Indicates prerenal cause for azotemia

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28
Q

Low BUN/Creatinine ratio

A

Indicate acute tubular necrosis, low protein intake, starvation or liver disease

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29
Q

eGFR

A

Indicates renal function
eGFR (mL/min/1.73m3) = 1.86 x
(Pcr)^-1.154 x(age)^-0.203 x (0.742 if female)
x (1.210 if AA)
> 60mL/min/1.73m^3

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30
Q

Total Protein Lab study

A

Measures numerous classes of proteins;
- Albumin
- Alpha-1 (AAT, A1-Fetoprotein)
- Alpha-2 (Haptoglobin, Ceruloplasmin)
- Beta (CRP, Transferrin, Complement)
- Gamma (Immunoglobulins)

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31
Q

Main protein in our bladder?

A

Albumin

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32
Q

Causes of Hyperproteinemia

A

Dehydration
Excess immunoglobulins - Multiple Myeloma, Waldenstrom’s macroglobulinemia

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33
Q

Causes of Hypoproteinemia

A

Kidney disease
Blood loss
Malnutrition
Liver disease

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34
Q

Causes of Hypoalbuminemia

A

Inflammation - negative APP (acute phase protein)
Hepatic
Urinary loss
GI loss
Poor diet

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35
Q

Compounds that are soluble in organic solvents and insoluble in water
- fats
- steroids

A

lipids

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36
Q

Synthesized in the liver and intestine
Constituent of cell membranes
Precursor for hormones
Transported by LDL and HDL

A

Cholesterol

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37
Q

Partially synthesized in liver
Transported by chylomicrons and VLDL
Provides energy to cells
Insulates organs

A

Triglycerides

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38
Q

Transport vehicles for lipids
- Chylomicrons
- VLDL; degrades to LDL in circulation
- LDL; “bad” - cholesterol into cells
- HDL; “good” - remove excess cholesterol from cells

A

Lipoproteins

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39
Q

Remove excess cholesterol from cells

A

High Density Lipoproteins

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40
Q

Transport cholesterol into cells

A

Low Density Lipoproteins

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41
Q

Hyperlipidemia may be caused by __________ via diet, diabetes, ETOH, hormone defect in pancreas, hypothyroidism

A

Increased Triglycerides

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42
Q

Hyperlipidemia may be caused by ________ via genetic defects in liver, lack of specific receptor on cells, diet

A

Increased Cholesterol

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43
Q

Causes of Hypolipoproteinemia

A

Genetic defect - low LDL/HDL

Absent LDL (w/low cholesterol)
- failure to thrive
- steatorrhea
- CNS degeneration
- malabsorption of fats and vitamins

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44
Q

Decreased LDL

A
  • increased life expectancy
  • decreased risk of CAD/AMI
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45
Q

Reduced HDL

A
  • increased risk of atherosclerosis/CAD
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46
Q

Absent HDL (Tangier’s disease)

A
  • increased accumulation of cholesterol in tonsils, adenoids and spleen
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47
Q

Included in Lipid Panel

A

Cholesterol
Triglycerides
HDL
LDL

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48
Q

Produced by catabolism of heme (RBC’s)

A

Bilirubin

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49
Q

_______ bilirubin is bound to glucuronide

A

Conjugated (direct)

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50
Q

Free bilirubin that has not been attached to a glucuronide molecule

A

Unconjugated (indirect) bilirubin

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51
Q

a yellow color in the skin, the mucous membranes, or the eyes

Due to -
Newborn (HDN)
Inherited
Hepatic dysfunction

A

Jaundice

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52
Q

Affects about 30% of breast-fed babies. Due to B-glucuronidase in breast milk
(deconjugates bilirubin)

A

Breast-milk jaundice

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53
Q

Inadequate milk supply

A

Breast-feeding jaundice

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54
Q

Thought to be caused by a deficiency in the enzyme glucuronosyltransferase. Inherited bilirubin disorder causing jaundice

A

Gilbert’s syndrome

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55
Q

Absence or deficiency of uridine diphosphate (UDP) glucuronyl transferase. Inherited bilirubin disorder causing jaundice.

A

Crigler-Najjar syndromes

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56
Q

Types of Liver disorders

A

Prehepatic
Hepatic
Posthepatic
-urinalysis can affect

57
Q

Function of Creatine Kinase (CK)

A

Production of ATP needed for muscle contraction

58
Q

____ is needed as a cofactor for creatine kinase (CK)

A

Mg2+

59
Q

Inhibitors of Creatine Kinase (CK)

A

Mn2+, Ca2+, Zn2+, Cu+
(Mg2+ in excess)

60
Q

Occurs as a dimer with two subunits (isoenzymes)

A

Creatine Kinase structure

61
Q

Brain type creatine kinase

A

CK-1(BB)

62
Q

hybrid type, cardiac tissue creatine kinase

A

CK-2(MB)

63
Q

muscle type (cardiac and skeletal) creatine kinase

A

CK-3 (MM)

64
Q

Percentage of serum CK fraction that is MM from skeletal muscle

A

98-100%

65
Q

Skeletal muscle CK distribution

A

CK-3 and CK-2

66
Q

Brain CK distribution

A

CK-1

67
Q

Heart CK distribution

A

CK-3 and CK-2

68
Q

Smooth muscle CK distribution

A

CK-1

69
Q

Devoid of CK

A

Liver and RBC’s

70
Q

May be indicated as increased CK-2. Can detect reinfarction soon after initial episode. Testing being replaced by troponins

A

Myocardial infarction

71
Q

can separate CK-MB into isoforms 1 & 2
- Clinical sensitivity @ 6hrs 90-95%
- Diagnostic specificity 89-100%

A

high voltage electrophoresis

72
Q

Muscle disease indicated by increased CK-3

A

Muscular dystrophy (Duchenne type)

73
Q

CNS disease indicated by increased CK-1 (70x)

A

Reye’s Syndrome

74
Q

Indicated by increased CK-3 (5x)

A

Hypothyroid

75
Q

CK is unstable above ____ degrees C. Best stored refrigerated or frozen. Not affected by slight hemolysis.

A

37

76
Q

Protein that regulates muscle contraction

A

Troponins

77
Q

How many subunits are there for Troponins?

A

3 - T,I,C

78
Q

94-97% of troponins are located in ______.

A

Myofibrils

79
Q

T and I subunits of troponins are useful in the diagnosis of _____.

A

AMI

80
Q

Troponins are more specific than CK-MB and are ______ in the serum of healthy and non-cardiac patients

A

Absent

81
Q

Levels become elevated 2-3 hrs after AMI
Can remain increased up to for 7-10 days after AMI
Clinical sensitivity of 50 - 75% up to 4-6 hours after onset of chest pain
High clinical sensitivity (>90%) up to 4-7 days after AMI

A

Troponins T and I

82
Q

Function of Lactate Dehydrogenase (LD/LDH)

A

H+ ion transfer enzyme w/ NAD as acceptor
Catalyzes the reversible reaction of pyruvate to lactate (based on pH)
L->P (pH 8.8-9.8)
P->L (pH 7.4-7.8)

83
Q

Fractions of LD. Present in all cells cytoplasm. Tissue levels are 500x higher than serum

A

5 major + LD-X and LD-6

84
Q

Isoenzyme of LD in mitochondria, 20-40% activity

A

LD-1 (HHHH)

85
Q

Isoenzyme of LD - major form in serum. 35-46%

A

LD-2 (HHHM)

86
Q

Isoenzyme of LD - 17-33%

A

LD-3 (HHMM)

87
Q

Isoenzyme of LD - 9-18%

A

LD-4 (HMMM)

88
Q

Isoenzyme of LD - major fraction in skeletal muscle (6-17%)
- Force conversion of pyruvate to lactate, regeneration of NAD
- Anaerobic glycolysis (cytoplasm)

A

LD-5 (MMMM)

89
Q

Cardiac tissue and RBC’s have the highest concentration of which lactate dehydrogenase isoenzyme

A

LD-1

90
Q

During AMI - LD rise within 12-24 hrs, peak within 48-72, may be elevated for 10 days
“______________”- 80% seen
Hemolysis (2 and 1 would flip flop to indicate MI)

A

Flipped pattern

91
Q

Elevated LD 1 and 2 indicates

A

Megaloblastic anemia

92
Q

10x total LD indicates

A

Liver; toxic hepatitis - lower in viral hepatitis
10x total LD indicates

93
Q

normal - 2x total LD indicates

A

Cirrhosis/Obstructive jaundice

94
Q

Germ cell tumors

A

elevated LD-1 indicates

95
Q

elevated total LD indicates

A

Malignant Diseases

96
Q

Elevated LD 2, 3 and 4 indicate

A

PLT destruction (ITP) (3 highest)
- Lymphatic system;
- Mono
- Lymphomas and leukemias

97
Q

Elevated LD 5 indicates

A
  • Liver disease
  • Passive congestion (CHF)
  • Skeletal injuries or disorders
98
Q

Increase in all levels but normal pattern

A
  • Hypoxia
  • Hyperthermia
  • Congestive heart failure
  • Renal Disease
99
Q

High LD activities will be seen in the _________ in 90% of bacterial infections
10% of viral infections
Specimen - free of hemolysis, separate from cells immediately

A

Cerebrospinal fluid

100
Q

Functions of Alkaline Phosphatase

A

nonspecific enzyme
- catalyzes the hydrolysis of many phosphomonoesters at an alkaline pH
- movement of substances across cell membranes
- lipid transport in GI
- calcifying process in bone

101
Q

Forms of Alkaline Phosphatase

A

Located at or in cell membranes
Major isoenzymes derived from liver, bone, intestine, placenta, spleen, and kidney (*most common elevation causes)

Placental (2nd and 3rd trimester)

102
Q

Primary areas where you’ll see elevated phosphate

A

Liver and Bone

103
Q

Present in most tissue
Liver - hepatocytes and biliary tract cells
Bone - osteoblasts (children and geriatrics)
Intestine - blood groups B or O who are secretors
Placenta; increased 1 - 1 ½ upper limit
- 16 - 20 weeks
Kidney

A

Distribution of Alkaline Phosphatase

104
Q

alkaline phosphatase abnormality of bone disease- osteoblast involvement (highest) 10-25x UL

A

Paget’s disease

105
Q

alkaline phosphatase abnormality of bone disease- moderate (2-4x UL)

A

Osteomalacia

106
Q

alkaline phosphatase abnormality of bone disease- normal to slight increase

A

Osteoporosis

107
Q

alkaline phosphatase abnormality of bone disease - high

A

Bone cancer

108
Q

alkaline phosphatase abnormality of liver disease ( >3x UL)

A

Extrahepatic obstruction

109
Q

alkaline phosphatase abnormality of liver disease (< 3x UL)

A

Intrahepatic obstruction

110
Q

alkaline phosphatase abnormality of liver disease (<3x to normal)

A

Viral hepatitis

111
Q

______ causes of increased synthesis of alkaline phosphatase -
pregnancy, healing fractures, infections

A

Transient

112
Q

alkaline phosphatase abnormality causing slight to moderate increase in levels.

A

Secondary Hyperparathyroidism

113
Q

The _____ type of amylase breaks 1,4 alpha linkages of sugars (random). This requires calcium and chloride.

A

Alpha

114
Q

Amylase is readily _____ by the kidneys and has a pH optimum at 6.9 - 7.0

A

Filtered

115
Q

Hydrolase; breakdown of polysaccharides, different rates

A

Functions of Amylase

116
Q
  • synthesized by acinar cells
  • involved in major digestion of starches
A

Pancreatic (p-type) amylase

117
Q
  • In the mouth
  • neutralized by stomach pH
A

Salivary (s-type) amylase

118
Q

Distribution of amylase

A

Small conc. in other tissues (ovaries, testes, tears, colostrum, lungs, adipose tissue)
Salivary glands (greatest conc.)
Pancreas

119
Q

Hyperamylasemia is seen in ______ in which serum levels rise w/in 5 - 8 hours of symptom onset
- 4-6x UL normal
- max conc. @ 12 - 72 hours
- RTN by day 3 - 4

A

Acute Pancreatitis

120
Q

Hyperamylasemia seen in this - up to 4x UL.

A

Cholesystitis

121
Q

Causes of Hyperamylasemia (levels not mentioned)

A

Obstruction
Salivary gland inflammation

122
Q

Hyperamylasemia seen in this - 50x UL

A

Carcinomas; lung and ovary

123
Q

Testing for hyperamylasemia can also detect

A
  • pseudocyst
  • ascites
  • pleural effusion
  • trauma
  • alcoholism
124
Q

Functions of Lipase

A

Hydrolyzes ester linkage of triglycerides to glycerol and fatty acids (carbons 1 & 3)
Bile salt and colipase assist in emulsification
Emulsification - fat to small sizes

125
Q

Lipase sources

A

Pancreas
Tongue

126
Q

Lipase increased levels seen in _______. Serum levels rise in 4-8hrs (2-50xUL), peak @ ~24hrs, decreases 8-14 days
Other causes;
- obstructions
More specific for pancreatitis than amylase levels.

A

Pancreatitis

127
Q

Transaminases

A

Catalyze the reversible transfer of an amine from an alpha-amino acid to an alpha-keto acid

Participate in amino acid catabolism and biosynthesis

128
Q

Alanine aminotransferase (ALT)

A

Catalyzes the reversible transfer of an amine group
Alanine + Oxoglutarate Pyruvate + glutamate

Widely distributed in tissues
Predominate source, liver & kidney

129
Q

ALT is _________ and indicates Liver cell damage (Hepatocellular disorders, ie. Hepatitis)

A

Liver Specific

130
Q

Aspartate + Oxoglutarate <-> oxaloacetate + glutamate
Tissue sources - widely distributed
- Heart and liver
- Skeletal muscle
- Kidney
Located in cytoplasm and mitochondria

A

Aspartate (AST)

131
Q

Significance of AST

A

Could be use to determine if pt was having AMI. Rise 6-8 hrs, peak at 18-48, normal 4-5 days (ALT usually normal)
- avg. increase 4-5x, 10-15x = fatal infarct
Muscular dystrophy - ~8x UL
Liver Diseases

132
Q

Gamma glutamyltransferase (GGT)

A

Transfer of gamma-glutamyl group from one peptide to another amino acid
Acts on glutamate residue
All cells (membrane) except muscle

133
Q

Function of Gamma glutamyltransferase (GGT)

A

Transport of amino acids through cell membrane
Serum levels originates in the liver
Kidney shows highest activity
Can be liver function test

134
Q

Significance of Gamma glutamyltransferase (GGT)

A

Elevated in all forms of Liver disease
- Hepatitis - moderate
- Liver cancer - high
- Cirrhosis - variable
Pancreatitis - 5-15x UL
Prostate malignancy
Anticonvulsant drugs

135
Q

Intrahepatic or posthepatic biliary obstruction (highest) 5-30x normal

More sensitive of an indicator than ALP, ALT, AST for obstructive jaundice, cholecystitis & cholangitis (occurs earlier and persists longer)

A

GGT and Biliary Obstruction

136
Q

Liver function tests (LFTs)

A

ALT
AST
GGT
Albumin/Total Protein
Bilirubin
ALP
PT

137
Q

Cardiac Panel

A

Troponin T and/or I
CK-MB
Total CK
Myoglobin
LD (1/2)?
AST?

138
Q

Pancreatic panel

A

Amylase
Lipase
Calcium
Triglycerides
Glucose

Clinical Chemistry (7 decks)

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