Diabetes and Other Carbohydrate Disorder

Report
MLAB 2401: Clinical Chemistry
Keri Brophy-Martinez
Diabetes and Other Carbohydrate
Disorders
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Hyperglycemia
Increase in plasma glucose
levels due to hormone
imbalance
Healthy patients
– Insulin is secreted by the β
cells of the pancreatic
islets of Langerhans
Reference Range
– Increased plasma glucose:
•
> 110 mg / dl
•
74 - 106 mg / dl
– Glucose reference range:
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Effects of Hyperglycemia
Immediate Effects
– Increased extracellular osmotic pressure
• The increased glucose in plasma pulls water out
of cells
• Results in dehydration
– Acidosis - metabolic acidosis.
• May result
• If the patient’s cells are not able to take in
glucose, they may begin to convert fats to fatty
acids, which then become keto acids.
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Effects of Hyperglycemia: Long term
Physiological
– Heart attacks/strokes, Diabetic
retinopathy(Blindness), kidney failure, neurologic
defects, susceptibility to infections
Chemical
– Glycosylated hemoglobin
• the formation of glycosylated hemoglobin is the result of
prolonged elevation of plasma glucose.
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Diabetes
Characterized by hyperglycemia
Disorders differ in etiology, symptoms and
consequences
Lab’s role
– Assist in diagnosis of the disease
– Identification of the disorder
– Assessment of progression of tissue damage
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Physiologic abnormalities of diabetes
Hyperglycemia
– increase blood glucose.
– Doesn’t matter how the glucose is derived - diet, fat
metabolism, protein destruction/wasting
Ketosis
– from fat metabolism, ketonemia, ketonuria
Hyperlipidemia -increase blood lipids from faulty glucose
metabolism.
Decrease blood pH - metabolic acidosis
Urine abnormalities
– Glycosuria – glucose present
– Polyuria - increase in urine volume
– Loss of electrolytes - washing out with the urine
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Diabetes
– World Health Organization (WHO) and American
Diabetes Association (ADA) recommends four
categories of diabetes:
• Type 1 diabetes
– Most severe and potentially lethal
• Type 2 diabetes
• Other (secondary diabetes)
• Gestational diabetes mellitus (GDM)
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Type 1 Diabetes
Insulin dependent diabetes mellitus ( IDDM )
5-10 % of diabetes cases
Demographics
– Non-Hispanic Whites/ Non-Hispanic Blacks
– Children & adolescents
Pathology
– Disease triggered by viral illness or environmental factors that
destroys beta cells in pancreas.
– Absolute Insulin deficiency
• Defect in secretion, production or action or all
• Autoimmune destruction of islet beta – cells in pancreas
• Auto-antibodies are present
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Type 1 Diabetes
Clinical Symptoms
– CLASSIC TRIAD
• Polyphagia (increased
food uptake)
• Polydipsia (thirst)
• Polyuria ( increased
urine production)
– Other symptoms
• Mental confusion
• Rapid weight loss
• Hyperventilation
• Diabetic ketoacidosis
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Laboratory Findings
Hyperglycemia- plasma levels > 110 mg/dL
Glucosuria- plasma glucose > 180 mg / dl
Decreased insulin
Increased glucagon
– Stimulation causes
• Gluconeogenesis
• Lipolysis (breakdown of fat produces ketones)
Ketoacidosis
Decreased blood pH ( acidosis )
 Sodium …  Potassium …  CO2
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Type II Diabetes
Non – Insulin Dependent Diabetes Mellitus( NIDDM )
Most common form of diabetes
Demographics
– Adult onset
– Patients usually > 20 years old
– American Indians and non-Hispanic blacks
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Type II Diabetes: Pathology
Develops gradually
Disorder in insulin resistance and relative
deficiency of insulin
Plasma glucose is unable to enter cells
Contributory factors
– Obesity
– Lack of exercise
– Diet
– Genetics
– Drugs, such as diuretics, psychoactive drugs
– Increases in hormones that inhibit/antagonize
insulin (GH & cortisol)
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Laboratory Findings
Hyperglycemia
Glucosuria
Insulin is present
Glucagon is not elevated
No lipolysis and no ketoacidosis
Excess glucose is converted to triglycerides (  plasma
triglycerides )
Normal / Increased Na / K
Increased BUN & Creatinine ( Decreased renal function )
Hyperosmolar plasma from hyperglycemia
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Other (SecondaryDiabetes)
Genetic defects of beta cell function
Genetic defects in insulin action
Genetic syndromes
Pancreatic disease
Endocrinopathies
Drug or chemical induced
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Gestational Diabetes
Glucose intolerance associated with pregnancy’s
hormonal and metabolic changes
Mothers usually return to normal after pregnancy, but with
increased risk for diabetes later on in life
Infants are at increased risk for respiratory complications
and hypoglycemia after birth
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Criteria for Diagnosis of Diabetes
1. Symptoms of diabetes plus random plasma glucose concentration > 200
mg/dL. Random is defined as any time of day without regard to time
OR
2. Fasting plasma glucose > 126 mg/dL. Fasting is defined as no caloric intake
for at least 8 hours.
OR
3. 2-Hour postprandial glucose > 200 mg/dL during an oral glucose tolerance
test
OR
4. A HgbA1C > 6.5%, confirmed on repeat measurement
Side notes
• Glucose tolerance testing ( GTT ) is considered to be of limited additional
use in the diagnosis of diabetes and not recommended, do 2 hour pp test
as stated above.
• Urine glucose testing is also not recommended in diabetes diagnosis
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Hypoglycemia
Plasma glucose level falls below 60 mg/dL
Glucagon is released when plasma glucose is < 70
mg / dL to inhibit insulin
Epinephrine, cortisol, and growth hormone released
from adrenal gland to increase glucose metabolism
and inhibit insulin
Treatment
– Varies with cause. Generally, hypoglycemia is
treated with small, frequent meals, (5-6 / day) low
in carbohydrates, high in protein
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Hypoglycemia
Symptoms
Increased hunger
Sweating
Nausea
Vomiting
Dizziness
Shaking
Blurring of speech
and sight
Mental confusion
Lab Findings
Decreased plasma
glucose
Whipple’s Triad
•Symptoms of hypoglycemia
•Low plasma glucose at time of
symptoms
•Alleviation of symptoms with
glucose ingestion
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Hypoglycemia
Causes of:
– Reactive
• Insulin overdose in diabetics
• Ethanol ingestion
– Fasting
• Insulin-producing tumors
• Hepatic dysfunction
• Sepsis
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Galactosemia
Resulting from :
–
Galactose 1, phosphate uridyl transferase deficiency
• enzyme that converts galactose to glucose, patients cannot
change either galactose or lactose into glucose.
• results in galactosemia (galactose in blood)
Effects:
– Can lead to mental retardation, cataracts, death
check children < 3 yrs for reducing substances
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References
Bishop, M., Fody, E., & Schoeff, l. (2010). Clinical Chemistry:
Techniques, principles, Correlations. Baltimore: Wolters Kluwer
Lippincott Williams & Wilkins.
Centers for Disease Control. (2012). Diabetes Public Health
Resource. Retrieved from
http://www.cdc.gov/diabetes/pubs/factsheet11.htm
Sunheimer, R., & Graves, L. (2010). Clinical Laboratory
Chemistry. Upper Saddle River: Pearson .
http://crossfitovercome.com/2011/12/29/diabetes-primer/
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