Clinical Chemistry I Exam 2

Front 1

Lipids are soluble in ______ but insoluble in _______

Back 1

organic solvents, water

Front 2

Lipids yield ______ or ______ on hydrolysis

Back 2

fatty acids or complex alcohols

Front 3

Four major functions of lipids

Back 3

biological membranes

efficient way to store excess calories

provide readily available energy reserves

serve as essential vitamins and hormones

Front 4

Fatty acids have what type of structure?

Back 4

R-COOH

Front 5

In nature, most fatty acids are ____ and have an ______ number of carbon atoms

Back 5

unsaturated, even

Front 6

Structure of triglycerides

Back 6

glycerol backbone with three fatty acids attached

Front 7

Most of the lipids that are obtained in the diet are _______

Back 7

triglycerides

Front 8

What type of bond is formed between the carboxylic acid of the fatty acid and the hydroxyl group of the glycerol backbone in triglycerides?

Back 8

ester bond

Front 9

Phospholipid structure

Back 9

2 esterified fatty acids (bound to glycerol) + phosphate + polar head group

Front 10

Cholesterol is a good source of energy (T/F)

Back 10

False, it is not easily broken down.

Front 11

Bile acids are more ______ than cholesterol

Back 11

polar

Front 12

Bile acids act as _______ in the intestine to break down ______.

Back 12

emulsifiers/detergents, dietary fat

Front 13

Lipoproteins are less water soluble than lipids (T/F)

Back 13

False, lipoproteins are more soluble due to the charge of the amino acids in the protein portion

Front 14

Which human plasma lipoprotein has the highest amount of protein?

Back 14

HDL

Front 15

HDL is also known as ______ lipoprotein

Back 15

alpha

Front 16

LDL is also known as _______ lipoprotein

Back 16

beta

Front 17

In a lipoprotein, more lipid means greater _______ and lower _______

Back 17

size, density

Front 18

In order to be transported in blood, lipids must combine with ________

Back 18

water-soluble compounds such as apolipoproteins

Front 19

Triglyceride must always be on the inside of lipoproteins because __________

Back 19

of their very hydrophobic nature

Front 20

Low-density lipoproteins are derived from _________

Back 20

VLDL by lipolysis

Front 21

What is lipoprotein (a)?

Back 21

LDL-like particles that are heterogeneous in size and density. They resemble plasminogen in structure and interfere with fibrinolysis. High plasma levels indicate higher risk for cardiovascular disease.

Front 22

High-density lipoprotein is capable of removing _________

Back 22

excess cholesterol from peripheral cells

Front 23

Apoproteins C and E are released when ______

Back 23

lipoprotein lipase forms LDL from VLDL

Front 24

Apoproteins associated with chylomicrons

Back 24

B48, C1-C3, E

Front 25

Apoprotein associated with LDL

Back 25

B100

Front 26

VLDL apoproteins

Back 26

B100, C1-C3, E

Front 27

HDL apoproteins

Back 27

A1, A2, C1-C3, E

Front 28

IDL apoprotein

Back 28

B-100

Front 29

Functions of apoproteins (for lipids)

Back 29

Activate enzymes involved in lipid metabolism, maintain structural integrity of lipid/protein complex, delivery of lipids to cells via recognition of cell surface receptors

Front 30

Four major pathways in lipoprotein metabolism

Back 30

Lipid absorption, Exogenous pathway, Endogenous pathway, Reserve cholesterol transport pathway

Front 31

Cholesteryl ester is hydrolzed by cholesterol esterase (pancreatic secretion) to form _________ and _______.

Back 31

free cholesterol, free fatty acid

Front 32

Triglycerides must be ______ before passing through the intestinal membrane

Back 32

hydrolyzed by lipase to free glycerol and fatty acids

Front 33

Lipase cannot directly attack triglyceride because of difference in ______

Back 33

charge, lipase is hydrophilic while triglyceride is hydrophobic

(bile acids solve this problem by forming micelles)

Front 34

Once the fatty acids and glycerol are inside the intestinal cell, _____ are reformed and combines with apoproteins to form _______

Back 34

triglycerides, chylomicrons

Front 35

Chylomicrons are transferred from intestinal cells to the _______

Back 35

lymphatic vessels

Front 36

All lipoprotein generated by the liver is in the form of _______

Back 36

VLDL

Front 37

Function of lecithin cholesterol acyltransferase. What is an important cofactor for this enzyme?

Back 37

Esterifies a fatty acid to a cholesterol molecule to allow import into cells. Apoprotein A-1.

Front 38

Atherosclerosis

Back 38

the deposition of lipids in various tissues within the body

Front 39

Risk factors for atherosclerosis

Back 39

>45 years men, >55 years women, family history, cigarette smoking, hypertension, diabetes mellitus, low HDL level, high LDL level, high total cholesterol, severe obesity, physical inactivity, stress

Front 40

Laboratory guidelines for desirable lipid levels

Back 40

Total cholesterol < 200 mg/dL
LDL < 100 mg/dL
HDL > 60 mg/dL

Front 41

Triglyceride level is not directly associated with risk of cardiovascular disease, but the recommended level is _______

Back 41

< 150 mg/dL

Front 42

Lipoprotein (a) desired level

Back 42

<30 mg/dL

(independent risk factor)

Front 43

How does lipoprotein (a) contribute to cardiovascular disease?

Back 43

Lp(a) has a structure very similar to plasminogen, and competes with plasminogen for activators, blocking their action. Plasmin is therefore unable to form and lyse clots.

Front 44

High HDL levels are associated with what populations?

Back 44

pre-menopausal women, people who exercise regularly, people with a low but healthy weight.

Front 45

Insulin, estrogen and thyroxine have what relationship with total cholesterol levels?

Back 45

Inverse

Front 46

How do statin drugs work?

Back 46

They inhibit HMG-CoA reductase (an enzyme which converts acetyl coA to cholesterol). This increases HDL and reduces LDL.

Front 47

How do fibrate drugs work?

Back 47

Activate LPL, promote rapid VLDL turnover, decrease VLDL secretion

However, these drugs are somewhat toxic to the liver

Front 48

Cholestyramine decreases plasma cholesterol by ________

Back 48

binding bile acids to prevent reabsorption by the liver

Not very well tolerated

Front 49

Hyperlipoproteinemia

Back 49

elevation of low density and high density lipoproteins

Primary: inborn error of metabolism
Seconday: diabetes, hormone replacement, nephrotic syndrome, hepatic disorder, blood pressure medication

Front 50

Hypertriglyceridemia primarily results from __________

Back 50

lipoprotein lipase deficiency

Front 51

The portal triad consists of

Back 51

a vein, an artery and a bile duct

Front 52

Reticuloendothelial cells break down hemoglobin into ________

Back 52

bilirubin

Front 53

Indirect or unconjugated bilirubin is bound to ________

Back 53

albumin

Front 54

Bilirubin diglucuronide is known as _________

Back 54

conjugated or direct bilirubin

Front 55

Urobilinogen may be excreted in ______

Back 55

urine or feces

Front 56

Jaundice

Back 56

excess bilirubin in body, can produce yellow pigment in skin or eyes

Front 57

Kernicterus

Back 57

Excess unconjugated bilirubin in brain tissue

Front 58

Delta bilirubin is ________

Back 58

a type of conjugated bilirubin that is bound to albumin covalently

Front 59

Unconjugated bilirubin is never excreted by the ______. This is because __________.

Back 59

kidney, the albumin molecule is too large to pass through the glomerulus

Front 60

Prehepatic jaundice is caused by _________.

Back 60

increased hemoglobin breakdown (i.e. hemolytic anemia, shortened hemoglobin lifespan, pernicious anemia)

Front 61

Prehepatic jaundice laboratory results

Back 61

Serum
indirect bilirubin increased
direct bilirubin normal

Urine
direct bilirubin negative
urobilinogen increased

Stool
urobilinogen increased

Front 62

Hepatic jaundice laboratory results (due to cell damage)

Back 62

Serum
increased indirect bilirubin
increased direct bilirubin

Urine
positive direct bilirubin
increased urobilinogen

Stool
variable urobilinogen

Front 63

Posthepatic jaundice laboratory results

Back 63

Serum
increased indirect bilirubin
increased direct bilirubin

Urine
direct bilirubin positive
decreased to negative urobilinogen

Stool
decreased to negative urobilinogen

Front 64

Causes of hepatic jaundice

Back 64

Conjugation failure, transport failure, cell damage

Front 65

Cause of post-hepatic jaundice

Back 65

obstruction of the bile duct

Front 66

Specimen requirements for bilirubin assay

Back 66

protected from light, serum/heparinized plasma, not hemolyzed

Front 67

The most common elevated element in hypercholesterolemia is _______ secondary to other disease

Back 67

LDL cholesterol

Front 68

Familial hypercholesterolemia is due to a defect or deficiency in ________

Back 68

LDL receptos

Front 69

Familial hypercholesterolemia results in an increased risk for ________

Back 69

atherosclerosis

Front 70

The treatment of choice for familial hypercholesterolemia is ______ because they decrease _______ LDL and increase _______

Back 70

statin drugs, endogenous, LDL receptors

Front 71

Triglceridemia may occur secondary to ______

Back 71

diabetes mellitus or hormonal abnormalities

Front 72

Severe hypertriglyceridemia may occur due to deficiency of ____ or _____

Back 72

LPL, apoprotein CII

Front 73

When LPL is absent, increased levels of chylomicrons cause lipemia even in fasting states (T/F)

Back 73

True, serum triglyceride levels may exceed 500 mg/dL

Front 74

Combined hyperlipoproteinemia consists of what?

Back 74

presence of increased serum cholesterol and triglyceride

Front 75

Familial combined hyperproteinemia is due to an overproduction of _____ and _____

Back 75

VLDL and B100

Front 76

Familial dysbetalipoproteinemia is due to _________ and results in increased _______ and _______

Back 76

presence of a rare form of apoE, VLDL, chlyomicron remnants

Front 77

Hypoalphalipoproteinemia is caused by

Back 77

decrease in HDL exhibited from absence or non-detectable levels of apo A-1.

Front 78

The sample of choice for analysis of lipids is ______

Back 78

serum

plasma with lithium heparin may also be used

Front 79

What is the minimum fast for a triglyceride sample?

Back 79

12 hour fast

Front 80

Is fasting necessary for cholesterol analysis?

Back 80

No, however fasting is necessary if a lipid panel is being performed

Front 81

Chylomicrons will be distributed throughout a serum sample (T/F)

Back 81

False, chylomicrons will generally float to the top. This is helpful in determining if a sample is fasting or not. Additionally, it is important to mix the sample well before analysis for this reason.

Front 82

HDL cholesterol analysis requires isolation of HDL by _______ of LDL/VLDL followed by ________. The supernatant HDL may then be measured with the same method as _______.

Back 82

precipitation, centrifugation, total cholesterol

Front 83

An alternative method of isolating cholesterol from HDL involves treatment of the serum with ______, which lyses HDL but _____ LDL and VLDL without lysis.

Back 83

a detergent, coats

Front 84

Friedewald formula

Back 84

total cholesterol = HDL + LDL + VLDL

Front 85

VLDL =

Back 85

triglyceride/5

as long as the sample is fasting (triglyceride < 400 mg/dL)

Front 86

Measurement methods for LDL

Back 86

direct immunoassay, ultracentrifugation

Front 87

In congestive heart failure, liver function is compromised by _______

Back 87

hypoxia

Front 88

Conjugated or direct bilirubin is ______ is water

Back 88

soluble

Front 89

Unconjugated or indirect bilirubin is _______ in water

Back 89

insoluble

Front 90

What enzyme is responsible for bilirubin conjugation?

Back 90

Uridyldiphosphate glucuronyl transferase

Front 91

Prehepatic jaundice results in increased ________ bilirubin

Back 91

unconjugated

Front 92

Total bilirubin reference range

Back 92

0.2 to 1.2 mg/dL

Front 93

Causes of prehepatic jaundice

Back 93

hemolytic anemia, ineffective erythropoiesis, neonatal physiological jaundice

Front 94

In prehepatic jaundice, bilirubin levels rarely exceed 5 mg/dL (T/F)

Back 94

True, this is because the liver is still functioning normally

Front 95

Unconjugated bilirubin (can/can not) cross the blood-brain barrier

Back 95

Can, this may result in kernicterus causing severe neurologic damage

Front 96

Treatment for neonatal physiological jaundice

Back 96

phototherapy with monochromatic blue like to oxidize bilirubin to more soluble end products to enhance renal excretion

Front 97

Intrahepatic jaundice

Back 97

problem is within the liver (impaired uptake, absent/decreased enzyme activity, defective excretion due to absence of transport molecule)

Liver enzymes ALT and AST will be highly elevated compared to LD

Front 98

Visible icterus occurs above ______ bilirubin

Back 98

3 mg/dL

Front 99

Posthepatic jaundice

Back 99

caused by physical barrier to bile excretion (obstructive, artesia), highly increased conjugated bilirubin, will be excreted in urine

Biliary enzymes will be elevated (GGT and ALP)

Front 100

Alcoholic jaundice is characterized by

Back 100

osmolalic increase, very high GGT (as compared to ALP)

Front 101

LD stands for

Back 101

Lactate dehydrogenase

Front 102

If true hepatic disease exists, what enzymes will be increased?

Back 102

AST, ALT, LD, usually with ALT>AST

Front 103

Decreased albumin is a very good marker for _______

Back 103

liver disease

Front 104

Amino acids are linked to each other through _____ bonds with the ______ group of one amino acid combining with the _______ group of another

Back 104

peptide, carboxyl, amino

Front 105

Aminoacidopathies

Back 105

inherited enzyme defects that inhibit metabolism of certain amino acids

cause several medical complications due to build-up of toxic amino acids and byproducts in blood

Front 106

For amino acid analysis in adults, sample should be collected in a tube containing ______ and should be drawn after a ________.

Back 106

lithium heparin, 6-8 hour fast

Front 107

______ may be used as a sample for screening amino acid analysis.

Back 107

Random urine

Front 108

Primary structure of a protein is determined by _________

Back 108

number and types of amino acids and their sequence in the polypeptide chain

Front 109

Tertiary structure is determined by ________

Back 109

the way the twisted chains or pleated sheets of amino acids fold back on themselves to form a 3D structure

Front 110

Zwitterion or ampholyte

Back 110

amino acid that at physiologic pH has both carboxyl and amino sites ionized

Front 111

Reference range for protein

Back 111

6.5-8.3 g/dL

Front 112

Factors influencing the rate of an enzymatic reaction

Back 112

pH, temperature, concentration of enzyme

Front 113

Increased temperature ________ the rate of an enzymatic reaction unless the temperature is too high (greater than 40 degrees celsius) which ________ the protein

Back 113

increases, denatures

Front 114

Hydrogen ion concentration changes the ionizable groups on enzymes and ______ the rate of the enzymatic reaction due to a change in ________

Back 114

decreases, shape of the protein

Front 115

Most enzymes work best between the pH of ____________. One exception is _______.

Back 115

7 to 8, gastric enzymes

Front 116

Ionic strength is the ____________

Back 116

cumulative concentration of all solutes

Front 117

Body enzymes are optimized for ______ conditions (osmolality)

Back 117

isotonic (300 mmol/L)

Front 118

A change in ionic strength changes the _______ of the medium in an enzymatic reaction, resulting in a _________ of the enzyme, resulting in a _________ rate of reaction.

Back 118

polarity, change in shape, decreased

Front 119

Enzymes are measured in terms of _______

Back 119

activity

international unit per liter = micromoles of substrate used up per minute of incubation per liter

Front 120

Enzyme concentration (zero order) =

Back 120

change in absorbance per minute/(extinction coefficient*length of light path) x 10^6 micromoles/mole x dilution factor

Front 121

Advantages of kinetic enzyme assay

Back 121

can inspect the data and use only the zero order reaction, can detect and eliminate lag phase or substrate exhaustion

Front 122

Advantage of one-point enzyme assay

Back 122

Faster, batching

Front 123

Name the three isoenzymes of CK and where each is found.

Back 123

CK-1 (BB) - brain and intestine
CK-2 (MB) - mostly cardiac muscle
CK-3 (MM) - skeletal and cardiac muscle

CK may also be found in the kidney, uterus, thyroid, liver and prostate.

Front 124

Total CK levels are always increased in ______ and ______. These enzymes are increased ______ the upper limit of normal.

Back 124

acute myocardial infarction, muscular dystrophy, 50-100x

Front 125

Reference range of CK

Back 125

25-170 U/L, slightly higher in men than women

Front 126

A hemolyzed sample will cause a falsely ______ value for CK due to the presence of ________

Back 126

increased, AK (similar enzyme)

Front 127

Isoenzymes of LD and where each is found

Back 127

LD1 - heart, RBC, kidney
LD2 - heart, RBC, kidney
LD3 - lungs
LD4 - liver/skeletal muscle
LD5 - liver
LD6 - CAD with liver disease

Front 128

Describe the change in LD in acute myocardial infarction

Back 128

LD1 > LD2

In health individuals, LD2 > LD1

Front 129

Reference range for LD

Back 129

100 - 225 U/L

Front 130

Aspartate aminotransferase is found in:

Back 130

liver, cardiac and skeletal muscle

Front 131

Aspartate aminotransferase increases in

Back 131

myocardial infarction (peaks @ 24 hours), pulmonary embolism, acute hepatocellular disorders (very high levels), skeletal muscle disorders

Front 132

Alanine aminotransferase is predominantly in the ______

Back 132

liver

Front 133

Alanine aminotransferase is ______ than AST in acute inflammatory conditions of the liver

Back 133

greater

Front 134

Oxidation of NADH + H+ results in a _______ in absorbance

Back 134

decrease

Front 135

Alkaline phosphatase is most significant in ______ and _____ disorders

Back 135

hepatobiliary, bone

Front 136

The Regan isoenzyme of ALP is a ________

Back 136

tumor marker

Front 137

Reference range for ALP

Back 137

30-90 U/L (can be as high as 125 depending on what method is used)

Front 138

Acid phosphatase is specific for the _______

Back 138

prostate gland

Front 139

Major significance of ACP is ________. However, it is not _______.

Back 139

prostatic carcinoma (particularly metastasized carcinoma), specific (mostly used to monitor therapy)

Front 140

Gamma-glutamyl transferase has clinical applications in ______ and _______ disorders.

Back 140

liver, biliary.

Front 141

_______ induces synthesis of GGT.

Back 141

alcohol abuse

Front 142

Amylase catalyzes the breakdown of ______ and ______

Back 142

starch, glycogen

Front 143

Amylase is utilized in the diagnosis of _________.

Back 143

acute pancreatitis

Front 144

Reference range of amylase

Back 144

35-125 U/L

Front 145

Lipase hydrolyzes __________

Back 145

ester linkages of fats to produce alcohols and fatty acids.

Front 146

An increase in lipase is specific for ________.

Back 146

pancreatitis

Front 147

Cholinesterase hydrolyzes _______.

Back 147

esters of choline to destroy poisons or drugs.

Front 148

Cholinesterase is found in ______, _____ and _______.

Back 148

liver, heart, white matter of brain

Front 149

Cholinesterase is a sensitive marker for ___________.

Back 149

organophosphate poisoning

Front 150

A decrease in cholinesterase is seen in ________, ______, ______ and _______.

Back 150

liver disease, starvation, burns and insecticide poisoning,

Front 151

ischemia

Back 151

lack of oxygenation due to interrupted blood flow to an organ

Front 152

angina pectoris

Back 152

chest pain from lack of oxygen to the heart muscle

characteristic crushing pain, often radiation to left arm, neck or shoulder blade

accompanied by sweating and "feeling of doom"

Front 153

arrythmia

Back 153

abnormal rhythm of heart beat due to abnormal stimulation or interruption of the nerve impulse

Front 154

myocardial infarction

Back 154

heart attack, necrosis of cardiac muscles due to interruption in blood flow and oxygen to the heart

Front 155

atherosclerosis

Back 155

hardening, roughing and narrowing of the blood vessels due to fatty plaque accumulation

Front 156

congestive heart failure

Back 156

inadequacy of pumping by the heart, decreased circulation of blood

Front 157

7 classic symptoms of heart disease

Back 157

dyspnea, chest pain, syncope, edema, cyanosis, fatigue, palpitations

Front 158

S-T elevation on an ECG is diagnostic for ________, however it is only seen in ______ of patients.

Back 158

myocardial infarction, 50%

Front 159

In myocardial infarction _____ > ______ (LD isoenzymes).

Back 159

LD1 > LD2

Front 160

CKMB is elevated _______ after myocardial infarction and peaks at _______.

Back 160

6-8, 18-24

Front 161

CKMB index =

Back 161

(CKMB activity/total CK activity) * 100

Reference range 1.5-6%

Front 162

CKMB levels return to normal _____ after MI.

Back 162

2-3 days

Front 163

Troponin I is the most sensitive and specific marker for _______

Back 163

myocardial infarction

Front 164

Troponin rises above normal level ______ after myocardial infarction

Back 164

6-8 hours

Front 165

Troponin peaks at ______ after myocardial infarction

Back 165

2-4 days

Front 166

Myoglobin increases ______ after myocardial infarction

Back 166

2-4 hours

Front 167

Myoglobin is an early marker for ______ but it is not ______.

Back 167

myocardial infarction, specific

Front 168

CRP is a marker for ______

Back 168

inflammation

Front 169

The level of CRP increases when in relationship to MI?

Back 169

a few hours to a few days before a heart attack

Front 170

Increased levels of homocysteine have recently been recognized as a _______

Back 170

cardiac risk factor

Front 171

An increase in homocysteine is correlated with _______

Back 171

damage to the endothelial lining of blood vessels

Front 172

In congestive heart failure, weakness in the left ventricle leads to ________.

Back 172

edema of the tissues

Front 173

Symptoms of CHF include

Back 173

edema, increase blood pressure, shortness of breath, easy fatigue, dizziness, difficulty in walking short distances, compromised renal function

Front 174

Patients who have had severed or repeated myocardial infarctions are at high risk for ________

Back 174

congestive heart failure

Front 175

B-type natriuretic peptide is a specific marker of ________

Back 175

edema due to heart failure

Front 176

BNP increases the _______ of the kidney to compensate for _________.

Back 176

urine output, fluid accumulation associated with CHF.

Front 177

Ischemia modified albumin

Back 177

when in contact with ischemic tissue, albumin is altered, decreasing its ability to bind certain metals (esp. cobalt)

Front 178

Separation techniques depend on differential ________.

Back 178

physical characteristics

Front 179

Common separation techniques in the clinical laboratory include _____ and ______.

Back 179

electrophoresis, chromatography

Front 180

Separation of charged particles during electrophoresis occurs because _________.

Back 180

different molecules move at different rates

Front 181

In electrophoresis, if the pH of the buffer is more basic than the pI, the protein carries a net _____ charge and will migrate to the ______.

Back 181

negative, anode (positive pole)

Front 182

Negatively charged molecules will move toward the _______ charged electrode known as the _____.

Back 182

positively, anode

Front 183

In addition to the electrical potential and the charge of the molecule, what forces can affect the movement of molecules in electrophoresis?

Back 183

Friction due to shape (symmetry) and size

Front 184

How is the voltage in the electrophoretic system chosen?

Back 184

to minimize heat and buffer evaporation while maximizing resolution

Front 185

The buffer in an electrophoretic system moves in the _____ direction to the flow of negatively charged sample molecules

Back 185

opposite

Front 186

Electroendoosmosis

Back 186

Large highly charged proteins may migrate towards the like-charged electrode because they absorb OH ions from the buffer

Front 187

Velocity of migration of molecules in electrophoresis is controlled by _________.

Back 187

the net charge of the particle, size and shape of the particle, strength of the electric field, chemical and physical properties of the supporting medium and electrophoretic temperature.

Front 188

Hepatic cirrhosis shows what patten on protein electrophoresis?

Back 188

beta-gamma bridging and decreased albumin peak

Front 189

Alpha-1-antitrypsin deficiency may cause what conditions?

Back 189

emphysema, hepatic cirrhosis

Front 190

A hemolyzed sample will cause what electrophoretic pattern?

Back 190

Free hemoglobin peak between alpha-2 and beta or
Hemoglobin-haptoglobin complex peak in the alpha-2 region

Front 191

(T/F) Significant protein is normally found in the urine

Back 191

False, protein in urine is usually in negligible amounts

Front 192

Elevated urine protein is an early indicator of ______.

Back 192

renal impairment

Front 193

What are Bence Jones proteins? They are present in what disorder?

Back 193

Ig light chains, multiple myeloma

Front 194

What is the proper sample for measurement of urine protein?

Back 194

24 hour urine collection

Front 195

What pattern will be seen in CSF electrophoresis in multiple sclerosis?

Back 195

oligoclonal banding of gamma proteins

Front 196

Major lipids

Back 196

fatty acids, triglyceride, cholesterol, cholesteryl esters, phospholipids, bile acids

Front 197

Cholesterol is slightly polar due to the ______

Back 197

free OH group at C3

Front 198

Cholesteryl ester is esterified at the _______

Back 198

C3-OH group

Front 199

Chylomicrons are _____ triglyceride and ______ cholesterol.

Back 199

84%, 7%

Front 200

VLDL is _____ triglyceride and ______ cholesterol

Back 200

44-60%, 16-22%

Front 201

IDL is ______ triglyceride and _____ cholesterol

Back 201

23%, 29%

Front 202

LDL is _______ triglyceride and ______ cholesterol

Back 202

11%, 62%

Front 203

HDL is _______ triglyceride and _______ cholesterol

Back 203

3%, 19%

Front 204

IDL and VLDL migrate near the ____ region in electrophoresis

Back 204

Pre-beta

Front 205

LDL is readily taken up via LDL receptors in ______ and ______ cells.

Back 205

liver, peripheral

Front 206

CETP

Back 206

plasma protein collects triglycerides from VLDL or LDL and exchanges them for cholesteryl esters from HDL, and vice versa.

Front 207

Insulin, estrogen and thyroxine have what type of relationship with total cholesterol level?

Back 207

inverse

Front 208

Hypoalphalipoproteinemia is associated with increased risk of ____ due to _____.

Back 208

CHD, build-up and blockage of blood vessels from excess LDL

Front 209

Hyperbetalipoproteinemia results in lack of _______ because of poor ______. This leads to _______.

Back 209

LDL uptake in steroid generating tissue, receptor specificity, deposition of cholesterol esters in tissues

Front 210

Triglyceride analysis reactions

Back 210

Detergent reagent breaks up lipoprotein particles into
their parts, releasing triglycerides into the solution

triglycerides + H2O + lipase yields fatty acids + glycerol

glycerol + ATP(Mg+2) + glycerol kinase yields glycerol-1-phosphate +ADP
 
glycerol-1-phosphate + O2 + glycerol phosphate oxidase yields DHAP + H2O2

H2O2 + 4-AAP + dye-precursor + peroxidase yields H2O + quinonimine dye (colored)

Front 211

Potential problems with triglyceride analysis

Back 211

free glycerol in the sample, standards are water soluble but triglyceride is water-insoluble (lipase and detergents must work), average molecular weight assumption, redox contaminants

Front 212

Total cholesterol analysis reactions

Back 212

detergent reagent breaks up lipoprotein particles into their parts, releasing cholesterol and cholesterol esters into the solution

cholesterol-ester + H2O + cholesterol esterase yields cholesterol + fatty acids

cholesterol + O2 + cholesterol oxidase yields cholestenone + H2O2

2H2O2 + reduced dye + peroxidase yields 4H2O + oxidized dye (colored)

Front 213

Problems in total cholesterol analysis

Back 213

interference from redox agents

Front 214

Define enzymes

Back 214

organic molecules that accelerate biochemical reactions

Front 215

Enzymes act as ______ and emerge from reactions ______.

Back 215

catalysts, unchanged

Front 216

Why does the clinical laboratory usually measure enzymes?

Back 216

To identify or monitor presence and amount of damaged tissue

Front 217

AST conducts what reaction?

Back 217

Transamination on aspartate

Front 218

Most transaminases require what cofactor?

Back 218

pyridoxal phosphate (a derivative of B6)

Front 219

Most oxidases use what as a cofactor?

Back 219

Oxygen

Front 220

Creatine kinase performs what reaction?

Back 220

Phosphorylation of creatine

Front 221

Amylase conducts what reaction?

Back 221

hydrolysis of starch (amylose)

Front 222

Alkaline phosphatase conducts what reaction?

Back 222

Removal of phosphate at alkaline pH

Front 223

Enzymes ____ the rate of reaction but do not change the ______.

Back 223

increase, equilibrium constant

Front 224

Enzymes work by _____ the activation energy of the reaction. This happens because enzymes form _____ with the substrate.

Back 224

decreasing, temporary intermediate bonds

Front 225

Enzymes reduce the ______ needed to activate reactions

Back 225

free energy

Front 226

Define zero-order kinetics

Back 226

Substrate concentration is high enough to saturate all enzyme present, reaction velocity is at max, rate is dependent only on enzyme concentration

Front 227

Michaelis-Menten equation

Back 227

V = Vmax[S] / (Km = [S])

Front 228

Lineweaver-Burk equation

Back 228

1/V = Km/Vmax[S] + 1/Vmax

Front 229

Y intercept of Lineweaver-Burk plot

Back 229

1/Vmax

Front 230

X-intercept of Lineweaver-Burk plot

Back 230

-1/Km

Front 231

Enzyme activity is extremely sensitive to its ______.

Back 231

shape

Front 232

Measurement Reaction for CK (from creatine)

Back 232

Creatine + ATP + CK ↔ Creatine phosphate + ADP

From ADP: (optimal pH = 9.0)
ADP + phophoenolpyruvate + PK ↔ pyruvate + ATP

Pyruvate + NADH + H+ + LD ↔ Lactate + NAD+

Front 233

Measurement reaction for CK (from creatine phosphate)

Back 233

(faster, optimal pH = 6.8)

Creatine phosphate + ADP + CK ↔ Creatine + ATP

ATP + Glucose + HK↔ Glucose- 6-phosphate + ADP

Glucose- 6-phosphate + NADP+ + G6PD ↔ 6-Phosphogluconate + NADPH + H+

Front 234

Sources of error for CK analysis

Back 234

hemolysis, exercise

Front 235

Measurement reaction of LD

Back 235

Lactate + NAD+ + LD ↔ Pyruvate + NADH + H+

Front 236

Sources of error in measuring LD

Back 236

hemolysis, refrigeration

Front 237

AST reference range

Back 237

15-30 U/L

Front 238

Measurement reaction of AST

Back 238

2-oxoglutarate + L-aspartate + AST ↔ L-glutamate + oxaloacetate

Oxaloacetate + NADH + H+ + MD ↔ NAD+ + L-Malate

Front 239

At what wavelength does NADH/NADPH have peak absorbance?

Back 239

340 nm

Front 240

AST must use ______ serum.

Back 240

non-hemolyzed

Front 241

ALT reference range

Back 241

6-37 U/L

Front 242

Increased levels of ALT are seen in what type of disorder?

Back 242

hepatocellular

Front 243

Measurement reactions for ALT

Back 243

alanine + alpha-ketoglutarate + ALT ↔ pyruvate + glutamate

pyruvate + NADH + H+ + LD ↔ lactate + NAD+

Front 244

4 major isoenzymes of ALP. These enzymes differ in _____ stability.

Back 244

bone, liver, placenta, intestine, heat

Front 245

Phenylalanine inhibits ____ and ____ isoenzymes of ALP more than ______ and ______.

Back 245

intestinal, placental, bone, liver

Front 246

Measurement reactions for ALP

Back 246

p-Nitropphenyl + ALP ↔ p-Nitrophenol + Phosphate ion

Increase in Abs. of p-nitrophenol is measured @ 405nm

Front 247

Sources of error for ALP measurement

Back 247

high fat, left at room temp or refrigerated

Front 248

ACP is measured by what reaction?

Back 248

p-nitrophenol reaction (pH = 5)

Front 249

What are potential sources of error for ACP measurement?

Back 249

hemolysis, sample left at room temperature (loss of CO2 resulting in pH change)

Front 250

Reference range of GGT

Back 250

up to 45 U/L

Front 251

In addition to alcohol abuse, what other conditions result in increased GGT?

Back 251

diabetes, MI, pancreatitis

Front 252

Measurement reactions for GGT

Back 252

gamma-glutamyl-p-nitroanilide + glycylglycine + GGT yields p-nitroaniline (colored dye) + gamma-glutamylglycylglycine

Front 253

Tissue sources of amylase

Back 253

salivary glands and pancreas

Front 254

Sources of error in amylase measurement

Back 254

high triglyceride, EDTA or citrate anticoagulant

Front 255

Lipase is specific for diagnosis of _____.

Back 255

acute pancreatitis

Front 256

Reference range for lipase

Back 256

10-200 U/L

Front 257

Measurement reaction for lipase

Back 257

triglycerides + lipase yields fatty acids + glycerol

glycerol + ATP(Mg+2) + glycerol kinase yields glycerol-1-phosphate + ADP

glycerol-1-phosphate + O2 + glycerol oxidase yields DHAP + H2O2

H2O2 + 4-AAP + dye-precursor yields H2O + quinonimine dye (colored)

Front 258

Source of error in cholinesterase measurement

Back 258

hemolysis (RBCs contain acetylcholinesterase)

Front 259

In the body, iron is utilized in what 3 types of molecules?

Back 259

enzymes, hemoglobin, myoglobin

Front 260

As iron decreases, hepcidin synthesis ______. This results in release of iron from the _____ and _______ absorption in the duodenum.

Back 260

decreases, spleen, increased

Front 261

What test is the gold standard for iron assessment?

Back 261

bone marrow examination

Front 262

The serum iron assessment is sensitive to ________

Back 262

mild iron deficiency

Front 263

Transferrin saturation

Back 263

The ratio of serum iron or iron-binding capacity

Serum iron/TIBC * 100

Front 264

Which assessment is the most accurate indicator of iron supply to bone marrow?

Back 264

Transferrin saturation

Front 265

The serum transferrin receptor assay determines the cells' ______. It becomes _______ in iron deficiency.

Back 265

need for iron, elevated

Front 266

The best diagnostic test for iron deficiency is _______ as it measures the _______ in the body.

Back 266

serum ferritin, iron stores

Front 267

R/F ratio

Back 267

sTfr/serum ferritin

used to provide estimate of iron stores

Front 268

Iron levels can become transiently increased by iron ingestion so samples should be fasting. (T/F)

Back 268

True. Additionally, iron has a diurnal variation so morning samples are best.

Front 269

Colorimetric iron measurement reactions

Back 269

Fe3+:Transferrin + acid yields Fe3+ + apotransferrin

Fe3+ + Reducing Agents yields Fe2+

Fe2+ + Complexing chromogen yields Colored complex

Front 270

TIBC measurement

Back 270

Saturate all binding sites with excess Fe+3
Remove excess unbound iron
Measure protein-bound iron (per iron method)
Various methods are used to remove the excess iron

Front 271

UIBC =

Back 271

TIBC - Serum iron

Front 272

Oral contraceptives can increase serum ____ levels

Back 272

transferrin

Front 273

UIBC measurement

Back 273

Adds a fixed amount (in excess) Fe+3 at a neutral pH to saturate iron binding sites

The uptake of iron by the unoccupied serum iron-binding sites is measured by a serum iron method as a decrease in free iron.

Front 274

Ferritin may be measured by ______.

Back 274

immunoassay

Front 275

Transferrin may be directly measured by _______.

Back 275

immunological methods

Front 276

Serum iron reference range

Back 276

50-160 micrograms/dL

Front 277

TIBC reference range

Back 277

250-410 micrograms/dL

Front 278

Laboratory results for iron deficiency anemia

Back 278

decreased serum iron, increased TIBC, decreased % saturation, decreased ferritin

Front 279

iron laboratory results for hemolytic anemia

Back 279

increased iron, decreased to normal TIBC, increased percent saturation, increased ferritin

Front 280

iron laboratory results for hemochromatosis

Back 280

increased serum iron, normal to decreased TIB, increased percent saturation, increased ferritin

Front 281

iron laboratory results for lead poisoning

Back 281

decreased serum iron, normal TIBC, normal to increased % saturation, normal to increased ferritin

Front 282

What is the normal blood lead level for children?

Back 282

<10 mcg/dL

Front 283

The free erythrocyte protoporphyrin assay is sensitive for low lead levels (T/F)

Back 283

False, this test is not sensitive below 35 mcg/dL

Front 284

Is the zinc protoporphyrin test specific for lead poisoning?

Back 284

No, this test is also sensitive for iron deficiency and anemia of chronic disease

Front 285

What enzymes of the heme synthesis pathway are blocked by lead poisoning?

Back 285

ALA dehydratase, coproporphyrinogen oxidase, ferrochelatase

Front 286

What treatment is curative for congenital erythropoietic porphyria?

Back 286

bone marrow transplant

Front 287

Define porphyrin

Back 287

cyclic compound formed by methylene linkage of 4 pyrrole rings

Front 288

Uro and coproporphyrinogens are soluble in _______.

Back 288

water

Front 289

protoporphyrin is soluble in ______.

Back 289

lipids

Front 290

Both porphyrinuria and porphyrinemia are (primary or secondary) conditions.

Back 290

secondary

Front 291

Categories of porphyrias

Back 291

hepatic, erythropoietic
cutaneous, acute

Front 292

Acute intermittent porphyria

Back 292

hereditary defect of hepatic porphobilinogen deaminase, increased delta-ALA in urine, increased porphobilinogen in urine

Front 293

Congenital erythropoietic porphyria

Back 293

Gunther's disease, deficiency in uroporphyrinogen III cosynthase, increased ALA, uroporphyrinogen and coproporphyrinogen

Front 294

Porphyria cutanea tarda

Back 294

Most common porphyria, deficiency of uroporphyrinogen carboxylase, hepatic, increased uroporphyrin in urine, normal ALA and PBG

Front 295

Watson-Schwatz test

Back 295

Tests for porphobilinogen

PBG + Ehrlich’s gives red color

Must do extractions to prevent interference

Front 296

Porphyrin test

Back 296

Add amyl alcohol, ethel ether and glacial acetic acid to urine

Shake, allow to separate

Upper, organic layer will fluoresce if porphyrins are present

Front 297

Reference range for free or zinc protoporphyrin

Back 297

20 – 80 μg/dL

Front 298

Serum level of LD peaks at _____ hours and returns to normal ____ to ____ days following AMI.

Back 298

12, 7-14

Front 299

Troponin levels return to normal _____ days after MI.

Back 299

5-10

Front 300

What compounds have been shown to help reduce homocysteine levels in the blood?

Back 300

B vitamins, folic acid

Front 301

In congestive heart failure, _____ slows, allowing _______ to accumulate in tissues.

Back 301

circulation, water/waste

Front 302

In patients with congestive heart failure, BNP serum levels are usually greater than _______.

Back 302

100 pg/mL