4) Carbohydrates Flashcards
critical low glucose
<40 mg/dL
RR glucose
74-100 mg/dL
critical high glucose
<400 mg/dL
fasting glucose normal
70-99 mg/dL
fasting glucose prediabetic
100-125 mg/dL
DM fasting glucose
≥126 mg/dL
2hr/random glucose normal
<140 mg/dL
2hr/random glucose prediabetic
140-199 mg/dL
2hr/random glucose DM
≥200 mg/dL
A1c normal
<5.7%
A1c prediabetic
5.7-6.4%
A1c DM
≥6.5%
OGTT criteria (50g drink)
≥140 g/dL
OGTT criteria (100g drink)
fasting ≥95 mg/dL
1 hour ≥180 mg/dL
2 hour ≥155 mg/dL
3 hour ≥140 mg/dL
gray tube
time limit
sodium fluoride
measure within 1 hour of draw
renal threshold for glucose
160-180 mg/dL
CSF glucose normal
RR
decreased levels indicate…
60-70% of serum glucose
50-80 mg/dL
infection
whole blood glucose is…
15% lower than serum glucose (less concentrated)
sample type for A1c
whole blood (purple top)
fasting glucose time period
8-10 hours
nothing but water PO
other body fluids glucose
90% of plasma glucose
formation of G6P from noncarb sources; ketone byproduct
gluconeogenesis
conversion of glucose to glycogen after heavy meal
glycogenesis
regulates glucose between meals
glycogenolysis
conversion of glucose or other hexoses into 3C molecules (lactate or pyruvate)
glycolysis
——- linkage forms disaccharides
glycosidic
> 10 monosaccharides linked
polysaccharide
glucose + fructose
sucrose
glucose + galactose
lactose
glucose + O2 + H2O → gluconic acid + H2O2
glucose oxidase
glucose + ATP → G6P + ADP
hexokinase
most accurate and common methodology for instruments
measures reducing substances in urine
primarily to detect galactosemia in children
CLINITEST/Benedict’s test
increase glucose levels by inhibiting insulin, glucagon, GH, and other hormones
from D cells of Islets
somatostatin
produced by adrenal medulla
fight or flight
inhibits insulin, increases plasma glucose
epinephrine
produced by adrenal cortex
stimulated by ACTH
increases plasma glucose
cortisol
produced by anterior pituitary
release cortisol
ACTH
produced by anterior pituitary
release stimulated by low glucose, low cortisol
GH
produced by thyroid
stimulated by TSH
increase plasma glucose
thyroxine
triiodothyronine
incomplete fat metabolism when carbs cannot be used
DM, starving, vomiting, glycogen storage disease
ketones
3 ketones
Beta-hydroxybutyrate 78%
acetoacetic acid 20%
acetone 2%
early indicator of kidney damage in DM
microalbuminuria
severe O2 deprivation
severe metabolic acidosis from DM
lactate
hyperosmolar state dilutes plasma
requires close monitoring in DKA
potassium and sodium
functions and examples of polysaccharides
storage + structural
starch
glycogen
cellulose
Catabolizes polysaccharides to intermediate-sized glucosans called “limit dextrins” and maltose
salivary amylase
Completes digestion of starch and glycogen to limit dextrins and maltose
pancreatic amylase
Secretes a group of 3 disaccharide enzymes (maltase, lactase, and sucrase)
intestinal mucosa
4 potential pathways for carbs
Converted to liver glycogen and stored
Metabolized completely to CO2 and H2O to provide immediate energy
Converted to keto acids, amino acids, and proteins
Converted to fats (triglycerides) and stored in adipose tissue
Oxidizes glucose to ribose and CO2
Formation of NADPH
pentose-phosphate pathway
(hexose monophosphate shunt)
Stored in secretory granules of the β-cells
proinsulin
proinsulin cleaved in equal molar amounts to…
insulin
C-peptide
check if insulin is endogenous or exogenous
C-peptide level
(should be = to endogenous insulin level)
Tumor of the pancreas that is derived from beta cells
insulinoma
Stimulates glycogenolysis, gluconeogenesis, and lipolysis (breakdown of fat)
Inhibits glycolysis, glycogenesis, and lipogenesis
glucagon
stress and exercise can induce secretion &
DM can impair secretion
glucagon
3 Ps of T1DM
Polydipsia: excessive thirst
Polyuria: increased secretion and discharge of urine
Polyphagia: increased appetite, eating large amounts of food
Most commonly occurs in patients with Type II diabetes with a concurrent acute febrile illness that leads to a reduced fluid intake
Hyperosmolar hyperglycemic state (HHS)
r/f for T2DM
- Age ≥ 45 years
- Overweight (BMI ≥ 25 kg/m2) or weight >120% of desirable body weight
- Family history of diabetes (parents or siblings with diabetes)
- Habitual physical inactivity
- Race/ethnicity: Hispanic, Native American, African American, Pacific Islander
- Previously identified Impaired Fasting Glucose (IFG) or Impaired glucose tolerance (IGT)
- History of GDM or delivery of a baby weighing > 9 lb
- HTN (≥ 140/90 in adults)
- HDL cholesterol ≤35 mg/dL and/or a triglyceride level ≥250 mg/dL
- PCOS
- History of vascular disease
medication often used for T2DM
metformin
secondary conditions to T2DM
- Heart disease is the leading cause of death in diabetics.
- High blood pressure is present in about 73% of diabetics.
- Heart disease and strokes occur two to four times more frequently due to arteriosclerosis because of hyperlipidemia
- Diabetic nephropathy occurs in 20-40% of diabetics
- Nervous system damage is present in 60 to 70% of diabetics.
- Susceptibility to infection with limb wounds/amptuations
Cushing’s
Acromegaly
Glucagonoma
Somatostatinoma
Hyperthyroidism
Certain drugs or chemicals
Genetic syndromes
causes of secondary DM
GDM screening time
24-28 weeks
non-DM causes of hyperglycemia
- Imbalance of the regulatory hormones
- Drugs (Corticosteroids, beta blockers, epinephrine, diuretics, statins, antipsychotics)
- Critical illness (Stroke, myocardial infarction, sepsis)
- Stress (Dysfunction of endocrine glands, pancreas issues, intracranial diseases)
drugs that can induce DM
Vacor
Nicotinic acid
Thyroid hormone
Thiazides
Dilantin
Glucocorticoids
4 tests for DM dx
Hemoglobin A1C
Fasting glucose
2-hour post load glucose
Random (casual) glucose
A1c measures…
glycated hemoglobin
average BG over last 2-3 months
OGTT
oral glucose tolerance test
child OGTT dose
1.75 g/kg body weight, not to exceed 75 grams
hypoglycemia BG
<50 mg/dL in men
<45 mg/dL in women
Weakness
Shakiness, nervousness
Rapid pulse, sweating
Hunger, epigastric discomfort
Lightheadedness, dizziness, confusion
Nausea, vomiting
Slurring of speech, blurring of sight
Loss of motor coordination
Unconsciousness
hypoglycemia
whipple’s triad for dx of hypoglycemia
- Signs and symptoms of hypoglycemia
- Documentation of low plasma glucose at the time patient is experiencing the signs and symptoms
- Alleviation of symptoms with the ingestion of glucose and an increase in plasma glucose
over 50% of hypoglycemia cases
mismanagement of DM with insulin
Diagnosed with a glucose level <50 mg/dL occurring after an overnight fast, between meals, or after physical activity.
Occurs within 12 hours of beginning a fast
Symptoms are usually neuroglycopenic and involve the central nervous system.
fasting hypoglycemia (pathologic)
Islet cell adenoma or carcinoma (insulinoma)
Non B cell tumors
Insulin-receptor antibody hypoglycemia
Surreptitious insulin injection/accidental insulin overdose
Severe liver disease
Severe renal disease
Septicemia
causes of fasting hypoglycemia
Usually benign and transient condition caused by excessive release of insulin from pancreas
Occurs 2-4 hrs after eating
Can be idiopathic, due to alimentary problems, or a result of congenital enzyme deficiencies
reactive/postprandial hypoglycemia (benign)
adrenergic sx of reactive hypoglycemia
Sweating, shakiness, nervousness, faintness, tachycardia, hunger
Hereditary fructose intolerance
Galactosemia
Alimentary hypoglycemia (gastrointestinal surgery: gastrectomy, gastrojejunostomy, pyloroplasty)
Adrenal insufficiency
Early onset type 2 diabetes mellitus
Idiopathic
causes of reactive hypoglycemia
glycogen storage disease
Deficiency of one of the 8 enzymes that break down glycogen (glycogenolysis) leading to a build up of glycogen
most common type of glycogen storage disease
Type I: Glucose-6-phosphatase deficiency, also known as von Gierke disease
Severe hypoglycemia occurs because glycogen cannot be converted back to glucose via hepatic glycogenolysis
type 1 glycogen storage disease
glycogen storage disease tx
avoid hypoglycemic events
liver transplant
type 1 glycogen storage disease dx
Failure of blood glucose to increase after galactose load
galactosemia
Lack of 1 of the 3 enzymes needed to metabolize galactose to glucose resulting in galactose in plasma
“Failure to thrive”, liver disease, cataracts, and (irreversible) mental retardation. Hypoglycemia may also develop
galactosemia
most common cause of galactosemia
galactose-1-phosphate uridyl transferase (Type 1)
glucose specimen handling
separate cells from plasma within 1 hour (5-7% decrease in glucose/hour)
sodium fluoride tube used if delay is necessary
CSF glucose term
glycorrhachia
sodium nitroprusside
ketone detection
Overproduction of ketones causes ketoacidosis, which results in a decreased ————- which therefore results in a decrease in blood pH.
(—— remains normal)
bicarbonate
pCO2
ketone sample handling
Must be tightly stoppered and analyzed immediately, or else falsely decreased results can occur (ketones are volatile)
must add glycine to detect acetone
a glucose molecule attached to the N-terminus of the B-polypetide chains of normal adult hemoglobin
HbA1C
5 types of A1c methodologies
High-performance liquid chromatography
Enzymatic
Capillary electrophoresis
Boronate affinity chromatography
Immunoassay
Used for patients who need to be monitored more frequently than once every 3 months (GDM, in therapy)
glycosylated albumin (fructosamine)
Non-enzymatic attachment of glucose to amino groups of proteins other than hemoglobin (serum proteins, membrane proteins, lens crystallins)
microalbuminuria defined as…
30-300 mg of albumin/24 hours
most sensitive microalbumin specimen
24 hour collection
Important for detecting and monitoring impaired circulatory and tissue oxygenation in critically ill DM patients
lactic acid
Collected in Gray top (Na fluoride), sent on ice, tested ASAP
lactic acid
