CHOs Flashcards
1
Q
General structures of CHOs, including formula
A
Composed of carbon, hydrogen, and oxygen in ratio of 1:2:1
- (CH2O)n
2
Q
What contains 3,4,5,6 or more carbon atoms
A
Monosaccharides
3
Q
Two monosaccharides linked together w/ the loss of a molecule of water
A
Disaccharides
4
Q
Composition of lactose
A
Glucose + galactose
5
Q
Composition of maltose
A
Glucose + glucose
6
Q
Composition of sucrose
A
Glucose + fructose
7
Q
Composition of glycogen
A
Multiple branches of glucose chains
8
Q
Reagent used to detect “reducing sugars”
A
Benedict’s reagent
9
Q
Composition of starch
A
Amylose and amylopectins (grains and starchy vegetables)
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)
11
Q
Two analogically important reducing sugars
A
Glucose and galactose
12
Q
Carb digestion
- Where does starch digestion begin and the enzyme responsible?
A
In the mouth by salivary amylase
13
Q
Digestion of starch due to ____ ____ in the intestine
A
Pancreatic amylase
14
Q
Four enzymes responsible for intestinal digestion
A
Lactase, maltase, sucrase, and galactase
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
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
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
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
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
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
21
Q
Specific site of production of insulin
A
Beta cells of islets of Langerhans of pancreas
22
Q
Function of C-peptide
A
To ensure correct structure of insulin
23
Q
Function of proinsulin
A
Storage form of insulin
24
Q
General effect of insulin on blood glucose concentration
A
Decrease
25
Four specific anabolic effects of insulin
↑ glycogenesis
↑ lipid synthesis (esp. triglycerides and cholesterol)
↑ glycolysis
↑ amino acid synthesis
26
Action of insulin on cell membranes and resultant effect on blood sugar levels
↑ in cell membrane permeabilty to glucose
↓ in blood levels of glucose
27
Specific effects of insulin on cells in the liver
Liver: INHIBITS glycogenolysis and gluconeogenesis and STIMULATES glycogenesis and fatty acid synthesis
28
Two specific catabolic effects of insulin
↓ hepatic glycogenolysis and gluconeogenesis
29
Major factor that regulates the release of insulin
Blood glucose concentration
- Insulin is released from pancreas when circulating blood glucose is increased
30
Specific site of glucagon production
Secreted by alpha cells of pancreatic islets of Langerhans
31
General effect of glucagon on blood glucose concentration
↑ blood glucose
32
Two specific glucose metabolism effects of glucagon
1. Stimulates glycogenolysis and gluconeogenesis to increase glucose
2. Inhibits glucose-consuming pathways in the liver
33
Major factor that regulates teh release of glucagon
Secreted when glucose is decreased
34
General effect on blood glucose concentration (increase or decrease) of:
- Growth hormone
Increased
35
General effect on blood glucose concentration (increase or decrease) of:
- Epinephrine
Increased
36
General effect on blood glucose concentration (increase or decrease) of:
- Adrenocorticotrophic hormone (ACTH)
Increased
37
General effect on blood glucose concentration (increase or decrease) of:
- Cortisol
Increased
38
General effect on blood glucose concentration (increase or decrease) of:
- Thyroxine (T4)
Increased
39
General effect on blood glucose concentration (increase or decrease) of:
- Somatostatin
↑ 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)
40
General effect on blood glucose concentration (increase or decrease) of:
- Somatomedins
↓ glucose
- produced in liver in response to stimulation by growth hormone
41
Hyperglycemia blood sugar value
Glucose \> 100 mg/dL
42
Hypoglycemia blood sugar value in adults
Glucose \< 50 mg/dL
43
Three specific diagnostic criteria for diabetes mellitus and specific laboratory values associated w/ the diagnostic criteria
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
44
Nine complications of diabetes
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
45
Four clinical symptoms used in the diagnosis of diabetes mellitus
1. Polyuria
2. Polyphagia
3. Polydipsia
4. Unexplained weight loss
46
One specific cause of Type 1 diabetes mellitus
Beta cell destruction
47
Five causes of beta cell injury in diabetes mellitus
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)
48
Relative insulin concentration in Type 1 diabetes mellitus
Decreased to absent insulin (absolute insulinopenia)
49
Three general metabolic changes in Type 1 diabetes mellitus
1. Inhibition of glycolysis
2. Increased glycogenolysis, lipolysis, and gluconeogenesis
3. Increased levels of acetyl CoA, converted to ketone bodies
50
Treatment of Type 1 diabetes mellitus
Administration of exogenous insulin injections
51
Type 2 diabetes mellitus
- 8 factors that predispose patients for the disease
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
52
Type 2 diabetes mellitus
- Two specific causes of the disease
Insuline resistance and beta cell failure
53
Type 2 diabetes mellitus
- Two factors that may predispose a patient to develop the disease
Genetic factors (stronger tendency than in Type 1) and environmental factors (obesity or increased caloric intake)
54
Type 2 diabetes mellitus
- Relative insulin concentrations
Variable (depends on cause and severity of disease)
55
Type 2 diabetes mellitus
- Treatment
1. Weight loss
2. Dietary changes
3. Oral hypoglycemia agents (Glucophage)
56
A form of glucose intolerance diagnosed in some women during pregnancy
Gestational diabetes mellitus (GDM)
57
Possible _long term_ effect of GDM
Women who had gestational diabetes have 35-60% chance of developing diabetes in the next 10-20 years
58
Screening test for gestational diabetes
O'Sullivan test
59
Caused by a single gene defect that causes faulty insulin secretion
Maturity-onset diabetes of youth (MODY)
60
Affected age group of MODY
Manifests before age 25
61
Four conditions that may cause secondary diabetes
1. Pancreatic disease
2. Cystic fibrosis
3. Corticosteroid administration
4. Hormonal disorders (Cushing's disease, acromegaly, etc.)
62
Two hour post-parandial blood sugar levels associated w/ impaired glucose levels
140-199 mg/dL
63
Fasting blood sugar levels in impaired glucose tolerance
Fasting plasma glucose \> 100 \< 125 mg/dL
64
Hemoglobin A1c level in prediabetes diagnosis
5.7-6.4%
65
Symptoms unique to adolescent diabetes mellitus
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
Definition of double (hybrid) diabetes
Child has elements of both Type 1 and Type 2 diabetes mellitus
67
How do patients develop double diabetes?
- Type 1 becomes overweight then becomes insulin dependent
- Type 2 develops Abs to beta cells
68
What is the most important factor in the development of diabetes mellitus?
Important factor is weight gain in diabetic adolescents
69
Typical blood glucose levels and clinical findings in hypoglycemia
Symptoms: weakness, shakiness, sweating, nausea, rapid pulse, lightheadness, epigastric discomfort
Fasting blood sugar \< 50 mg/dL
70
Severe hypoglycemia
- Cause
- Typical blood glucose concentration
- Caused by severe CNS dysfunction
- Blood sugar \< 20-30 mg/dL
71
Hypoglycemia in neonates and infants
- Cause
- Typical blood glucose concentration
- Due to low glycogen stores at birth
- Blood glucose at approximately 35 mg/dL
72
Fasting hypoglycemia in adults
- Cause
- Typical blood glucose concentration
- 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
Reactive hypoglycemia
- Cause
- Typical blood glucose concentration
- Occurs in everyday life after eating
- Postprandial symptoms if glucose is \< 45-50 mg/dL
- Must rule out fasting hypoglycemia first
74
Specific enzyme defect in galactosemia
Galactase deficiency
75
Clinical symptoms and long-term effects of galactosemia
- Infants who fail to thrive on cow's milk; vomiting and diarrhea
- Later, can cause liver disease, cataracts, and mental retardation
76
3 laboratory means of galactosemia diagnosis
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
Specific enzyme deficiency of lactose intolerance
Lactase deficiency
78
Clinical symptoms of lactose intolerance
1. Abdominal pain
2. Diarrhea
3. Lactose in urine
79
Specific cause of glycogen storage diseases
Caused by deficiencies of a specific enzyme in glycogen metabolism
80
What are the 3 liver forms of glycogen storage diseases?
What are their 4 general clinical biochemical features?
- Types I, IV, and VI
- Are characterized by hepatomegaly, hypoglycemia, decreased insulin, and increased glucagon
81
What are the 4 muscle forms of glycogen storage disease?
What is 1 general clinical feature of the muscle forms of glycogen storage disease?
- Types II, III, V, and VII
- Appear in young adulthood during strenuous exercise
82
Specific enzyme deficiency in von Gierke's disease
Deficiency of glucose-6-phosphatase
83
Is von Gierke's disease a liver or muscle form of a glycogen storage disease?
Liver form (most common and most severe form)
84
Specific enzyme deficiency in Pompe's disease?
Deficiency of alpha-1,4-glucosidase
85
Is Pompe's disease a liver or muscle form of a glycogen storage disease?
Muscle form
86
Why should separation from the cells or testing must be performed w/in a half hour of venipuncture in glucose testing?
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
Why is oxalate-sodium fluoride the preferred anticoagulant in glucose testing?
Oxalate-sodium fluoride (gray top) inhibits enolase, a critical enzyme in the glycolytic pathway
88
Whole blood glucose value
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
Plasma glucose value
70-100 mg/dL
90
Oxygenated, deoxygenated, and capillary blood glucose value
Oxygenated and capillary values are 2-5 mg/dL higher than deoxygenated samples
- This makes a huge difference in pediatric heel stick samples
91
What is the reason for the prompt analysis of CSF glucose?
Due to possible cellular utilization and resultant false picture
92
What is the relationship normally observed b/w plasma glucose and CSF glucose?
CSF is lower than plasma glucose (60-70%) at the same time
93
Clinical significance for urine glucose
- Specific renal threshold range for urine glucose
Glucose appears in urine after blood glucose exceeds renal threshold
- Renal threshold: 160-180 mg/dL
94
What are the 3 copper reductase methods for glucose?
1. Benedicts test (Clinitest)
2. Somogyi-Nelson
3. Neocuproine Copper Reduction
95
Benedict's Copper Reduction Test (Clinitest)
- Principle of measurement
Based on the reduction of cupric iron in supric sulfate; change in absorbance is measured
96
Benedict's Copper Reduction Test (Clinitest)
- Clinical significance of a positive test
Used as a screen for diseases of inborn errors of CHO metabolism in newborns
97
Benedict's Copper Reduction Test (Clinitest)
- Specific CHOs detected
Galactose and glucose
98
Benedict's copper reduction test (Clinitest)
- Interferences
Includes false positives from other sugars, ascorbic acid, salicylates, penicillin, and uric acid
99
A two step reaction that is proposed to be the reference method when a protein-free filtrate is used
Hexokinase
100
Hexokinase reagents and products
Reagent: Hexokinase and glucose-6-phosphate dehydrogenase
Products: Glucose6-phosphate and 6-phosphoglyconate +NADPH + H+
101
The first step of hexokinase is ____ while the second is \_\_\_\_
Specific; non-specific
102
Absorbance in hexokinase is measured at \_\_\_\_
340 nm
103
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
Glucose oxidase; "Trinder"
104
Glucose oxidase "Trinder" reagents
Glucose oxidase; peroxidase
105
Plasma glucose reference interval
- Adult
70-100 mg/dL
106
Plasma glucose reference interval
- Children
70-100 mg/dL
107
Plasma glucose reference interval
- Preemies
25-80 mg/dL
108
Plasma glucose reference interval
- Term babies
60-95 mg/dL
109
CSF glucose reference interval
60-70% of concommitant plasma levels
110
Whole blood glucose reference interval
- Adults
60-90 mg/dL
111
Urine glucose reference interval
- Random
- 24 hours
- 30 mg/dL for random urine glucose
- \< 500 mg/24 hours
112
Patient preparation instructions for an oral glucose tolerance test (OGTT)
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
3 indications for performing an intravenous glucose tolerance test
1. Malabsorption
2. Sprue (celiac disease)
3. GI surgery
114
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
Postprandial testing; \> 126 mg/dL
115
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
O'Sullivan test; 24-28 weeks; 50g; \> 140 mg/dL
116
Metabolic pathway that leads to ketone body formation
Formed from beta-oxidation of free fatty acids
117
Name 3 ketone bodies and their specific relative proportions in the blood
1. Beta-hydroxybutyric acid (78%)
2. Acetoacetic acid (20%)
3. Acetone (2%)
118
Specific starting points of ketone bodies
Pyruvate, amino acids, and fatty acids
119
3 processes that lead to ketosis due to patient's deficiency of glucose
Decreased sodium, decreased bicarbonate, and decreased blood pH
120
Why does the patient develop acidosis and hyperlipidemia?
The body is using fatty acids as energy in hyperlipidemia
Increased in free ketone bodies produces exess H+ ions in acidosis
121
5 conditions of decreased CHO availability that can lead to ketosis
1. Starvation
2. Frequent vomiting
3. Glycogen storage diseases
4. Alkalosis
5. Alcoholism
122
Specific reagent used in colorimetric method (Acetest or Ketostix)
Sodium nitroprusside
123
Specific realtive activity w/ each of the three ketone bodies in the colorimetric method
Reacts ONLY w/ acetone and acetoacetate; 5x more sensitive to acetactate; does NOT react w/ beta-hydroxybutyrate
124
Specimen storage requirements for the colorimetric method (Acetest/Ketostix)
1. Keep container closed (volatile analyte)
2. Keep refrigerated (any microbes present will use up ketone bodies causing a false negative result)
125
Describe the pathogenies of hyperosmolar hyperglycemic nonketonic come (HHNC)
1. Occurs in older patients
2. Increased blood glucose (no ketosis)
3. Increased osmolality
4. Intracellular dehydration
5. Cellular edema in the brain
126
Three causes of Type A lactic acidosis
Decreased tissue oxygenation from:
- Shock
- Hypovolemia
- Cardiac failure
127
Five causes of Type B lactic acidosis
Metabolic causes associated w/ disease (diabetes mellitus, neoplasia, liver diseases) or drugs/toxins (alcohol, salicylates)
128
Five causes of increased CSF lactate
- Levels should parallel blood values
1. CVA
2. Intracranial hemorrhage
3. Bacterial meningitis (nromal in viral)
4. Epilepsy
5. Other CNS disorders
129
Patient preparation, specimen collection, and sample analysis requirements for lactate
- No tourniquet
- No exercising of arm
- Must be placed on ice IMMEDIATELY
- Separate from cells w/in 15 minutes of draw
130
Discuss the process of glycation
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
Why can the measurement for glycated hemoglobin be used to assess diabetic blood sugar control over a 3-4 month at a time span?
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
Two general categories of glycated hemoglobin measurement methods
1. Methods based on charge differences (ion exchange chromatography, HPLC, ELP)
2. Methods based on structural differences (immunoassay and affinity chromatography)
133
Specific clinical application of measuring
- Insulin
Evaluates fasting hypoglycemia; not necessary to measure to diagnose diabetes mellitus
134
Specific clinical application of measuring:
- Proinsulin
Evaluates patients with benign or malignant beta-cell tumors of pancreas
135
Specific clinical application of measuring:
- C-Peptide (3)
Evaluates fasting hypoglycemia, insulin-producing beta-cell tumors, response to pancreatic surgery
136
Specific clinical application of measuring:
- Urine glucose (via dipstick)
Uses glucose oxidase to produce color change; specific for glucose only
137
Specific importance of urinary albumin and miroalbumin measurements in predicting diabetic nephropathy
Persistent proteinuria is the best indicator for renal disease and can be used to screen diabetics for nephropathy development
138
Importance of urinary micro albumin excretion
It precedes nephropathy and is a marker for mirovascular disease!
139
140
Excess of glucose in the bloodstream outside of reference range; often associated w/ diabetes mellitus
Hyperglycemia
141
Abnormally low blood glucose level
Hypoglycemia
142
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
- 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
Specific effects of insulin on cells in the muscle
Muscle: STIMULATES glycogenesis, glucose uptake and metabolism, amino acid uptake, and protein synthesis and INHIBITS protein catabolism and amino acid release
144
Specific effects of insulin on cells in the adipose tissue
Adipose tissue: STIMULATES glycerol and fatty acid synthesis and INHIBITS lipolysis
