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Liz's Clinical Chemistry Module 1 > CHOs > Flashcards

CHOs Flashcards

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1
Q

General structures of CHOs, including formula

A

Composed of carbon, hydrogen, and oxygen in ratio of 1:2:1

  • (CH2O)n
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2
Q

What contains 3,4,5,6 or more carbon atoms

A

Monosaccharides

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3
Q

Two monosaccharides linked together w/ the loss of a molecule of water

A

Disaccharides

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4
Q

Composition of lactose

A

Glucose + galactose

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5
Q

Composition of maltose

A

Glucose + glucose

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6
Q

Composition of sucrose

A

Glucose + fructose

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7
Q

Composition of glycogen

A

Multiple branches of glucose chains

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8
Q

Reagent used to detect “reducing sugars”

A

Benedict’s reagent

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9
Q

Composition of starch

A

Amylose and amylopectins (grains and starchy vegetables)

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10
Q

Significance of a positive test for reducing sugars

A

Galactose isn’t detected by a dipstick

  • Therefore, if urine is negative for glucose w/ a dipstick but is positive w/ a Clinitest, they have galactose in urine (galactosemia)
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11
Q

Two analogically important reducing sugars

A

Glucose and galactose

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12
Q

Carb digestion

  • Where does starch digestion begin and the enzyme responsible?
A

In the mouth by salivary amylase

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13
Q

Digestion of starch due to ____ ____ in the intestine

A

Pancreatic amylase

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14
Q

Four enzymes responsible for intestinal digestion

A

Lactase, maltase, sucrase, and galactase

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15
Q

What organ do these metabolic pathways occur in and specific starting and ending products

  • Glycolysis (anaerobic and aerobic)
A

Breakdown of glucose (glucose → lactate ↔ pyruvate)

  • Anaerobic: glucose → lactate/RBCs and skeletal muscle
  • Aerobic: pyruvate → acetyl CoA/mitochondria
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16
Q

What organ do these metabolic pathways occur in and specific starting and ending products:

  • Glycogenesis
A

Making glycogen (glucose-1-phosphate → glycogen)

  • Occurs when there’s a decrease in blood glucose concentration
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17
Q

What organ do these metabolic pathways occur in and specific starting and ending products

  • Kreb’s cycle (oxidative phosphorylation)
A

??

  • Pyruvate → acetyl CoA → ATP, CO2, water
  • Occurs in the mitochondria
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18
Q

What organ do these metabolic pathways occur in and specific starting and ending products:

  • Glycogenolysis
A

Breaking down glycogen

  • Glycogen → glucose-1-phosphate → glucose
  • Occurs in muscle and liver tissues during a time of fasting
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19
Q

What organ do these metabolic pathways occur in and specific starting and ending products:

  • Gluconeogenesis
A

Making new glucose from non-CHO sources

non-CHO sources → glucose

(non-CHO sources are amino acids, lactate, glycerol, and fatty acids)

  • Occurs in the liver
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20
Q

What organ do these metabolic pathways occur in and specific starting and ending products:

  • Hexose monophosphate pathway
A

??

  • Glucose-6-phosphate → ribose + CO2
  • Occurs in the liver
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21
Q

Specific site of production of insulin

A

Beta cells of islets of Langerhans of pancreas

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22
Q

Function of C-peptide

A

To ensure correct structure of insulin

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23
Q

Function of proinsulin

A

Storage form of insulin

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24
Q

General effect of insulin on blood glucose concentration

A

Decrease

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25
Q

Four specific anabolic effects of insulin

A

↑ glycogenesis

↑ lipid synthesis (esp. triglycerides and cholesterol)

↑ glycolysis

↑ amino acid synthesis

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26
Q

Action of insulin on cell membranes and resultant effect on blood sugar levels

A

↑ in cell membrane permeabilty to glucose

↓ in blood levels of glucose

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27
Q

Specific effects of insulin on cells in the liver

A

Liver: INHIBITS glycogenolysis and gluconeogenesis and STIMULATES glycogenesis and fatty acid synthesis

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28
Q

Two specific catabolic effects of insulin

A

↓ hepatic glycogenolysis and gluconeogenesis

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29
Q

Major factor that regulates the release of insulin

A

Blood glucose concentration

  • Insulin is released from pancreas when circulating blood glucose is increased
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30
Q

Specific site of glucagon production

A

Secreted by alpha cells of pancreatic islets of Langerhans

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31
Q

General effect of glucagon on blood glucose concentration

A

↑ blood glucose

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32
Q

Two specific glucose metabolism effects of glucagon

A
  1. Stimulates glycogenolysis and gluconeogenesis to increase glucose
  2. Inhibits glucose-consuming pathways in the liver
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33
Q

Major factor that regulates teh release of glucagon

A

Secreted when glucose is decreased

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34
Q

General effect on blood glucose concentration (increase or decrease) of:

  • Growth hormone
A

Increased

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35
Q

General effect on blood glucose concentration (increase or decrease) of:

  • Epinephrine
A

Increased

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36
Q

General effect on blood glucose concentration (increase or decrease) of:

  • Adrenocorticotrophic hormone (ACTH)
A

Increased

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37
Q

General effect on blood glucose concentration (increase or decrease) of:

  • Cortisol
A

Increased

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38
Q

General effect on blood glucose concentration (increase or decrease) of:

  • Thyroxine (T4)
A

Increased

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39
Q

General effect on blood glucose concentration (increase or decrease) of:

  • Somatostatin
A

↑ glucose

  • Secreted by delta cells of pancreatic islets of Langerhans; inhibit both glucagon and insulin from pancreas (which ↓ glucose)
  • Can also inhibit growth hormone release (which ↑ glucose)
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40
Q

General effect on blood glucose concentration (increase or decrease) of:

  • Somatomedins
A

↓ glucose

  • produced in liver in response to stimulation by growth hormone
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41
Q

Hyperglycemia blood sugar value

A

Glucose > 100 mg/dL

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42
Q

Hypoglycemia blood sugar value in adults

A

Glucose < 50 mg/dL

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43
Q

Three specific diagnostic criteria for diabetes mellitus and specific laboratory values associated w/ the diagnostic criteria

A
  1. Fasting blood glucose > 126 mg/dL
  2. 2 hour post-parandial (2 HPP) glucose > 200 mg/dL during OGTT
  3. Clinical symptoms and random glucose > 200 mg/dL
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44
Q

Nine complications of diabetes

A
  1. Nephrophy (renal failure)
  2. Neuropathy (impaired sensation of feet)
  3. Heart disease and stroke
  4. Hypertension
  5. Blindness and retinopathy
  6. Amputations
  7. Dental disease
  8. Complications of pregnancy (birth defects, spontaneous abortion, excessively large baby)
  9. Life-threatening events
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45
Q

Four clinical symptoms used in the diagnosis of diabetes mellitus

A
  1. Polyuria
  2. Polyphagia
  3. Polydipsia
  4. Unexplained weight loss
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46
Q

One specific cause of Type 1 diabetes mellitus

A

Beta cell destruction

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47
Q

Five causes of beta cell injury in diabetes mellitus

A
  1. Genetic factors (HLA Ags on chromosome 6)
  2. Environmental factors
  3. Viral causes (measles, mumps, EBV, etc.)
  4. Chemical causes
  5. Autoimmune disease (85-90% of cases have detectable Abs)
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48
Q

Relative insulin concentration in Type 1 diabetes mellitus

A

Decreased to absent insulin (absolute insulinopenia)

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49
Q

Three general metabolic changes in Type 1 diabetes mellitus

A
  1. Inhibition of glycolysis
  2. Increased glycogenolysis, lipolysis, and gluconeogenesis
  3. Increased levels of acetyl CoA, converted to ketone bodies
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50
Q

Treatment of Type 1 diabetes mellitus

A

Administration of exogenous insulin injections

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51
Q

Type 2 diabetes mellitus

  • 8 factors that predispose patients for the disease
A
  1. Older age (> 40 years old)
  2. Obesity (BMI > 30)
  3. Family history
  4. Sex (females more prevalent than males)
  5. History of gestational diabetes
  6. Impaired glucose metabolism
  7. Physical inactivity
  8. Race/ethnicity
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52
Q

Type 2 diabetes mellitus

  • Two specific causes of the disease
A

Insuline resistance and beta cell failure

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53
Q

Type 2 diabetes mellitus

  • Two factors that may predispose a patient to develop the disease
A

Genetic factors (stronger tendency than in Type 1) and environmental factors (obesity or increased caloric intake)

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54
Q

Type 2 diabetes mellitus

  • Relative insulin concentrations
A

Variable (depends on cause and severity of disease)

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55
Q

Type 2 diabetes mellitus

  • Treatment
A
  1. Weight loss
  2. Dietary changes
  3. Oral hypoglycemia agents (Glucophage)
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56
Q

A form of glucose intolerance diagnosed in some women during pregnancy

A

Gestational diabetes mellitus (GDM)

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57
Q

Possible long term effect of GDM

A

Women who had gestational diabetes have 35-60% chance of developing diabetes in the next 10-20 years

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58
Q

Screening test for gestational diabetes

A

O’Sullivan test

59
Q

Caused by a single gene defect that causes faulty insulin secretion

A

Maturity-onset diabetes of youth (MODY)

60
Q

Affected age group of MODY

A

Manifests before age 25

61
Q

Four conditions that may cause secondary diabetes

A
  1. Pancreatic disease
  2. Cystic fibrosis
  3. Corticosteroid administration
  4. Hormonal disorders (Cushing’s disease, acromegaly, etc.)
62
Q

Two hour post-parandial blood sugar levels associated w/ impaired glucose levels

A

140-199 mg/dL

63
Q

Fasting blood sugar levels in impaired glucose tolerance

A

Fasting plasma glucose > 100 < 125 mg/dL

64
Q

Hemoglobin A1c level in prediabetes diagnosis

A

5.7-6.4%

65
Q

Symptoms unique to adolescent diabetes mellitus

A

They’re the same as adults, but also:

  • Blurred vision
  • Slow wound healing
  • Acanthosis nigricans (skin around neck or armpits appears dark, thick, and velvety)
  • Frequent infections
  • Hypertension
66
Q

Definition of double (hybrid) diabetes

A

Child has elements of both Type 1 and Type 2 diabetes mellitus

67
Q

How do patients develop double diabetes?

A
  • Type 1 becomes overweight then becomes insulin dependent
  • Type 2 develops Abs to beta cells
68
Q

What is the most important factor in the development of diabetes mellitus?

A

Important factor is weight gain in diabetic adolescents

69
Q

Typical blood glucose levels and clinical findings in hypoglycemia

A

Symptoms: weakness, shakiness, sweating, nausea, rapid pulse, lightheadness, epigastric discomfort

Fasting blood sugar < 50 mg/dL

70
Q

Severe hypoglycemia

  • Cause
  • Typical blood glucose concentration
A
  • Caused by severe CNS dysfunction
  • Blood sugar < 20-30 mg/dL
71
Q

Hypoglycemia in neonates and infants

  • Cause
  • Typical blood glucose concentration
A
  • Due to low glycogen stores at birth
  • Blood glucose at approximately 35 mg/dL
72
Q

Fasting hypoglycemia in adults

  • Cause
  • Typical blood glucose concentration
A
  • Caused by certain drugs (most common), toxins, advanced liver disease, hormone deficiencies, isulinomas, septicemia, and end-stage renal failure
  • Blood glucose < 45 mg/dL
73
Q

Reactive hypoglycemia

  • Cause
  • Typical blood glucose concentration
A
  • Occurs in everyday life after eating
  • Postprandial symptoms if glucose is < 45-50 mg/dL
  • Must rule out fasting hypoglycemia first
74
Q

Specific enzyme defect in galactosemia

A

Galactase deficiency

75
Q

Clinical symptoms and long-term effects of galactosemia

A
  • Infants who fail to thrive on cow’s milk; vomiting and diarrhea
  • Later, can cause liver disease, cataracts, and mental retardation
76
Q

3 laboratory means of galactosemia diagnosis

A
  1. Screening urine for reducing substances via Benedict’s test (Clinitest)
  2. ID of the sugar by paper
  3. Direct assay of enzyme activity
77
Q

Specific enzyme deficiency of lactose intolerance

A

Lactase deficiency

78
Q

Clinical symptoms of lactose intolerance

A
  1. Abdominal pain
  2. Diarrhea
  3. Lactose in urine
79
Q

Specific cause of glycogen storage diseases

A

Caused by deficiencies of a specific enzyme in glycogen metabolism

80
Q

What are the 3 liver forms of glycogen storage diseases?

What are their 4 general clinical biochemical features?

A
  • Types I, IV, and VI
  • Are characterized by hepatomegaly, hypoglycemia, decreased insulin, and increased glucagon
81
Q

What are the 4 muscle forms of glycogen storage disease?

What is 1 general clinical feature of the muscle forms of glycogen storage disease?

A
  • Types II, III, V, and VII
  • Appear in young adulthood during strenuous exercise
82
Q

Specific enzyme deficiency in von Gierke’s disease

A

Deficiency of glucose-6-phosphatase

83
Q

Is von Gierke’s disease a liver or muscle form of a glycogen storage disease?

A

Liver form (most common and most severe form)

84
Q

Specific enzyme deficiency in Pompe’s disease?

A

Deficiency of alpha-1,4-glucosidase

85
Q

Is Pompe’s disease a liver or muscle form of a glycogen storage disease?

A

Muscle form

86
Q

Why should separation from the cells or testing must be performed w/in a half hour of venipuncture in glucose testing?

A

Glucose decreases up to 7% per hour or more when serum is left in contact w/ cells

  • But if collected in a gold top w/ serum separator, we’re good
87
Q

Why is oxalate-sodium fluoride the preferred anticoagulant in glucose testing?

A

Oxalate-sodium fluoride (gray top) inhibits enolase, a critical enzyme in the glycolytic pathway

88
Q

Whole blood glucose value

A

60-90 mg/dL

  • Values are 12-15% less than plasma b/c plasma is more concentrated in the same amount of specimen volume compared to whole blood
89
Q

Plasma glucose value

A

70-100 mg/dL

90
Q

Oxygenated, deoxygenated, and capillary blood glucose value

A

Oxygenated and capillary values are 2-5 mg/dL higher than deoxygenated samples

  • This makes a huge difference in pediatric heel stick samples
91
Q

What is the reason for the prompt analysis of CSF glucose?

A

Due to possible cellular utilization and resultant false picture

92
Q

What is the relationship normally observed b/w plasma glucose and CSF glucose?

A

CSF is lower than plasma glucose (60-70%) at the same time

93
Q

Clinical significance for urine glucose

  • Specific renal threshold range for urine glucose
A

Glucose appears in urine after blood glucose exceeds renal threshold

  • Renal threshold: 160-180 mg/dL
94
Q

What are the 3 copper reductase methods for glucose?

A
  1. Benedicts test (Clinitest)
  2. Somogyi-Nelson
  3. Neocuproine Copper Reduction
95
Q

Benedict’s Copper Reduction Test (Clinitest)

  • Principle of measurement
A

Based on the reduction of cupric iron in supric sulfate; change in absorbance is measured

96
Q

Benedict’s Copper Reduction Test (Clinitest)

  • Clinical significance of a positive test
A

Used as a screen for diseases of inborn errors of CHO metabolism in newborns

97
Q

Benedict’s Copper Reduction Test (Clinitest)

  • Specific CHOs detected
A

Galactose and glucose

98
Q

Benedict’s copper reduction test (Clinitest)
- Interferences

A

Includes false positives from other sugars, ascorbic acid, salicylates, penicillin, and uric acid

99
Q

A two step reaction that is proposed to be the reference method when a protein-free filtrate is used

A

Hexokinase

100
Q

Hexokinase reagents and products

A

Reagent: Hexokinase and glucose-6-phosphate dehydrogenase

Products: Glucose6-phosphate and 6-phosphoglyconate +NADPH + H+

101
Q

The first step of hexokinase is ____ while the second is ____

A

Specific; non-specific

102
Q

Absorbance in hexokinase is measured at ____

A

340 nm

103
Q

A two-step reaction with the first step being specific and the second, non-specific

  • Good method for serum, plasma, urine, and csf
  • O-dianisidine is the chromogen
A

Glucose oxidase; “Trinder”

104
Q

Glucose oxidase “Trinder” reagents

A

Glucose oxidase; peroxidase

105
Q

Plasma glucose reference interval

  • Adult
A

70-100 mg/dL

106
Q

Plasma glucose reference interval

  • Children
A

70-100 mg/dL

107
Q

Plasma glucose reference interval

  • Preemies
A

25-80 mg/dL

108
Q

Plasma glucose reference interval

  • Term babies
A

60-95 mg/dL

109
Q

CSF glucose reference interval

A

60-70% of concommitant plasma levels

110
Q

Whole blood glucose reference interval

  • Adults
A

60-90 mg/dL

111
Q

Urine glucose reference interval

  • Random
  • 24 hours
A
  • 30 mg/dL for random urine glucose
  • < 500 mg/24 hours
112
Q

Patient preparation instructions for an oral glucose tolerance test (OGTT)

A
  1. Minimum of 150 g CHO for 3 days prior to the test
  2. Fasting for 10-16 hours (water only)
  3. Discontinue medications that alter glucose levels
  4. Normal amount of activity before and during test
113
Q

3 indications for performing an intravenous glucose tolerance test

A
  1. Malabsorption
  2. Sprue (celiac disease)
  3. GI surgery
114
Q

Can be used for preliminary diagnosis of diabetes mellitus; give 75 g oral glucose load or have patient a meal; 2 hours later if glucose is ____, may be diabetic

A

Postprandial testing; > 126 mg/dL

115
Q

Used to diagnose gestational diabetes, performed at ____ to ____ weeks gestation; give ___ g glucose load to fasting patient and draw sample at 1 hour; if ____ mg/dL performe OGTT

A

O’Sullivan test; 24-28 weeks; 50g; > 140 mg/dL

116
Q

Metabolic pathway that leads to ketone body formation

A

Formed from beta-oxidation of free fatty acids

117
Q

Name 3 ketone bodies and their specific relative proportions in the blood

A
  1. Beta-hydroxybutyric acid (78%)
  2. Acetoacetic acid (20%)
  3. Acetone (2%)
118
Q

Specific starting points of ketone bodies

A

Pyruvate, amino acids, and fatty acids

119
Q

3 processes that lead to ketosis due to patient’s deficiency of glucose

A

Decreased sodium, decreased bicarbonate, and decreased blood pH

120
Q

Why does the patient develop acidosis and hyperlipidemia?

A

The body is using fatty acids as energy in hyperlipidemia

Increased in free ketone bodies produces exess H+ ions in acidosis

121
Q

5 conditions of decreased CHO availability that can lead to ketosis

A
  1. Starvation
  2. Frequent vomiting
  3. Glycogen storage diseases
  4. Alkalosis
  5. Alcoholism
122
Q

Specific reagent used in colorimetric method (Acetest or Ketostix)

A

Sodium nitroprusside

123
Q

Specific realtive activity w/ each of the three ketone bodies in the colorimetric method

A

Reacts ONLY w/ acetone and acetoacetate; 5x more sensitive to acetactate; does NOT react w/ beta-hydroxybutyrate

124
Q

Specimen storage requirements for the colorimetric method (Acetest/Ketostix)

A
  1. Keep container closed (volatile analyte)
  2. Keep refrigerated (any microbes present will use up ketone bodies causing a false negative result)
125
Q

Describe the pathogenies of hyperosmolar hyperglycemic nonketonic come (HHNC)

A
  1. Occurs in older patients
  2. Increased blood glucose (no ketosis)
  3. Increased osmolality
  4. Intracellular dehydration
  5. Cellular edema in the brain
126
Q

Three causes of Type A lactic acidosis

A

Decreased tissue oxygenation from:

  • Shock
  • Hypovolemia
  • Cardiac failure
127
Q

Five causes of Type B lactic acidosis

A

Metabolic causes associated w/ disease (diabetes mellitus, neoplasia, liver diseases) or drugs/toxins (alcohol, salicylates)

128
Q

Five causes of increased CSF lactate

  • Levels should parallel blood values
A
  1. CVA
  2. Intracranial hemorrhage
  3. Bacterial meningitis (nromal in viral)
  4. Epilepsy
  5. Other CNS disorders
129
Q

Patient preparation, specimen collection, and sample analysis requirements for lactate

A
  • No tourniquet
  • No exercising of arm
  • Must be placed on ice IMMEDIATELY
  • Separate from cells w/in 15 minutes of draw
130
Q

Discuss the process of glycation

A

Glycation is the non-enzymatic addition of a sugar residue to amino groups of protein

  • Glucose binds reversibly to accessible amino groups on hemoglobin to form a labile aldimine; aldomine intermediates form a stable ketoamine (irreversible “Amadori” rearrangement); conformation change of glucose to cyclic structures occurs
131
Q

Why can the measurement for glycated hemoglobin be used to assess diabetic blood sugar control over a 3-4 month at a time span?

A

Since glycated hemoglobin formation is irreversible AND the normal RBC lifespan is 120 days, these tests assess diabetic compliance with therapy for the preceding 120 days! Levels are unaffected by day-to-day fluctuation, exercise, etc

132
Q

Two general categories of glycated hemoglobin measurement methods

A
  1. Methods based on charge differences (ion exchange chromatography, HPLC, ELP)
  2. Methods based on structural differences (immunoassay and affinity chromatography)
133
Q

Specific clinical application of measuring

  • Insulin
A

Evaluates fasting hypoglycemia; not necessary to measure to diagnose diabetes mellitus

134
Q

Specific clinical application of measuring:
- Proinsulin

A

Evaluates patients with benign or malignant beta-cell tumors of pancreas

135
Q

Specific clinical application of measuring:
- C-Peptide (3)

A

Evaluates fasting hypoglycemia, insulin-producing beta-cell tumors, response to pancreatic surgery

136
Q

Specific clinical application of measuring:
- Urine glucose (via dipstick)

A

Uses glucose oxidase to produce color change; specific for glucose only

137
Q

Specific importance of urinary albumin and miroalbumin measurements in predicting diabetic nephropathy

A

Persistent proteinuria is the best indicator for renal disease and can be used to screen diabetics for nephropathy development

138
Q

Importance of urinary micro albumin excretion

A

It precedes nephropathy and is a marker for mirovascular disease!

139
Q
A
140
Q

Excess of glucose in the bloodstream outside of reference range; often associated w/ diabetes mellitus

A

Hyperglycemia

141
Q

Abnormally low blood glucose level

A

Hypoglycemia

142
Q

Be able to draw and label 3-hour OGTT curves associated w/ a normal patient, a patient w/ diabetes mellitus, and an impaired glucose tolerance patient

A
  • DM: FBS ≥ 126 mg/dL; glucose > 200 mg/dL
  • IGT: FBS 101-125 mg/dL; at 2 hours back to FBS; never exceed 200 mg/dL
  • Normal: FBS 70-100 mg/dL; at 2 hours back to FBS; never exceed 200 mg/dL
143
Q

Specific effects of insulin on cells in the muscle

A

Muscle: STIMULATES glycogenesis, glucose uptake and metabolism, amino acid uptake, and protein synthesis and INHIBITS protein catabolism and amino acid release

144
Q

Specific effects of insulin on cells in the adipose tissue

A

Adipose tissue: STIMULATES glycerol and fatty acid synthesis and INHIBITS lipolysis

Liz's Clinical Chemistry Module 1 (5 decks)

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