Carbs Part 2 Flashcards
Hypoglycemia
< 80mg/ dL
Hyperglycemia
> 120mg/dL
HYPOGLYCEMIA
Insulin overdose
Postprandial hypoglycemia
Fasting hypoglycemia
Reactive hypoglycemia
Insulin overdose
GI surgery
Mild diabetes
Baba ang glucose after eating
Postprandial hypoglycemia
Insulin producing pancreatic islet tumor (insulinomas)
Hepatic dysfunction
ROH consumption
Fasting hypoglycemia
It refers to a group of common metabolic disorders that share the phenotype of hyperglycemia
Diabetes mellitus (DM)
Factors contributing to hyperglycemia include:
o reduced insulin secretion
o decreased glucose utilization
o increased glucose production
DM classification
PATHOGENESIS
B-Cell destruction
Absolute insulin deficiency
Autoantibodies
Type 1
DM classification
Insulin resistance with an insulin
secretory defect
Relative insulin deficiency
Type 2
DM classification
Glucose intolerance during pregnancy
Due to metabolic and hormonal
changes
Gestational
Autoantibodies
• Islet cell autoantibodies
• Insulin autoantibodies
• Glutamic acid decarboxylase autoantibodies
• Tyrosine phosphatase IA-2 and IA-2B autoantibodies
1.EXCESSIVE URINATION
2.INCREASED APPETITE
3.EXCESSIVE THIRST
POLYURIA
POLYPHAGIA
POLYDIPSIA
SYMPTOMS OF DIABETES
Always tired
Frequent urination
Always hungry
Sudden weight
Sexual problems
Always thirsty
Wounds that won’t heal
Blurry vision
Vaginal infections
Numb or tinglino hands or feet
o result of interactions of genetic, environmental, and immunologic factors that ultimately lead to the destruction of the pancreatic beta cells and insulin deficiency.
o It can develop at any age, develops most commonly before____ years of age.
DM T1
20
Autoantigen
Activation of T helper 1 lymphocytes
IFNy
Activation of______ with release of IL-1 and TNF o.
macrophages
Autoantigen
Activation of T helper 1 lymphocytes
IL-2
Activation of____
autoantigen-specific T cytotoxic (CD8) cells
Autoantigen
Activation of T helper 2 lymphocytes
IL-4
Activation of______ to produce islet cell autoantibodies and antiGAD65 antibodies
B lymphocytes
characterized by impaired insulin secretion, insulin resistance, excessive hepatic glucose production, and abnormal fat metabolism.
DM T2
As insulin resistance and compensatory hyperinsulinemia progress, the pancreatic islets in certain individuals are unable to sustain the hyperinsulinemic state.
DM T2
Insulin resistance
Compensatory B-cell hyperplasia
B-cell failure (early)
B-cell failure (late)
Normoglycemia
Impaired glucose tolerance
Diabetes
RISK FACTORS FOR TYPE 2 DIABETES
Have a family history of diabetes
Have a BMI ≥ 23.0 kg/m
Lead an inactive lifestyle
Have high blood pressure
Have abnormal blood cholesterol/lipid levels
Have a history of gestationa diabetes
Are > 40 years old
Have impaired glucose tolerance or impaired fasting glucose
Management of Type 2 Diabetes
Glycemic control
• Diet/lifestyle
• Exercise
• Medication
Management of
Type 2 Diabetes
Treat associated conditions
• Dyslipidemia
• Hypertension
• Obesity
• Coronary heart disease
Risk factors of DM T1
Genetic, autoimmune, environmental
Risk factors for DM T2
Genetic, obesity, sedentary lifestyle, race/ethnicity, hypertension, dyslipidemia, polycystic ovarian syndrome
Destruction of pancreatic beta cells, usually autoimmune
DM T1
No autoimmunity
DM T2
C peptide
Very low or undetectable
DM T1
C peptide
Detectable
DM T2
Therapy to prevent or delay DM T1
None known Clinical trials in progress
Therapy to prevent or delay DM T2
Lifestyle (weight loss and increased physical activity)
Oral medications (metformin, acarbose) may be helpful.
Medication therapy for DM T1
Insulin absolutely necessary; multiple daily injections or insulin pump
Medication therapy for DM T2
Oral agents and/or noninsulin injectable hypoglycemic drugs
Insulin commonly needed
DM T3 resembles
DM T2
What resembles DM T1
DM 3c
Pancreas experience damage
any degree of glucose intolerance
with onset or first recognition during pregnancy
Causes metabolic and hormonal
changes
Gestational Diabetes
Gestational DM
what trimester
2nd trimester (6 months)
T or F
Insulin does not cross the placenta, but glucose can!
True
GENETIC DEFECTS IN CHO METABOLISM
• Classic disorders of carbohydrate metabolism result from a specific enzyme defect
•________\ inheritance
Autosomal recessive
Affected tissue
Liver, intestine, kidney
Enzyme defect
Glucose-6-phosphatase
(Von Gierke’s disease)
Liver, muscle, heart
Lysosomal a-glucosidase
Pompe’s diseases
Liver, muscle
Amylo-1, 6-glucosidase
Forbe’s disease
Liver
1,4-0-glucan branching enzyme
Andersen disease
Muscle only
Phosphorylase
McArdle disease
Galactose-1-phosphate uridyl transferase
Classic galactosemia
Type I
Galactokinase deficiency
Type II Galactokinase
Galactose epimerase deficiency
Type II UDP galactose epimerase
Essential fructosuria
Hereditary fructose intolerance
FBPase deficiency
Fructokinase
Aldolase B
FBPase
