diabetes flashcards
(55 cards)
what are the cardinal signs or “polys” for diabetes? specifically type 1
polydipsia (excessive thirst)
polyuria (excessive urination)
polyphagia (constant hunger/big appeptite)
what are the diagnostic criteria for diabetes? A1C, FBG, OGTT, random plasma glucose
A1C >6.5
Fasting blood glucose > 126 mg/dL
2hr OGGT >200 mg/dL
random glucose >200 mg/L
What are characteristics of type I diabetes mellitus?
complete glucose intolerance
no functioning insulin-secreting pancreatic beta cells
dependent on exogenous insulin; tendency toward ketoacidosis
early age of onset (autoimmune)
family history often negative
What are common autoantibodies found in type I diabetics?
ICA- islet cell cytoplasmic autoantibodies
IAA- insulin autoantibodies
What does presence of c-peptide indicate in a diabetic?
Indicates that some beta cell mass is left; beta cells are still secreting insulin
At what point does a type I diabetic begin to have abnormal FBG?
When >70% of beta cell mass is lost
What autoantigens are most associated with type I diabetes?
Islet antigen 2 (IA-2), phogrin (IA-2B), zinc transporter, glutamic acid decarboxylase, voltage gated Ca2+, vesicle-associated membrane protein2 (VAMP- 2)
What are characteristics of non-obese diabetes mellitus?
very small percent (10%)
onset around 25; maturity onset diabetes of the young
yes family history
low insulin secretion (insufficient for glycemic control)
includes mutations in specific proteins
What are characteristics of obese diabetes mellitus?
largest % of population (80%)
onset usually over 35yo
yes family history
insulin secretion low for body mass
insulin resistance in tissues + decreased BCM
What are consequences of lack of insulin?
hyperglycemia (decreased glucose uptake in cells, decreased glycogen synthesis, increased conversion of amino acids to glucose–ketoacidosis)
glucosuria (glucose in the urine)
hyperlipidemia (fatty acid mobilization from fat cells; ketoacidosis)
uninhibited glucagon (increased glucagon levels even with increased blood glucose levels)
What are complications of diabetes?
cardiovascular micro and macro angiopathies
Neuropathy
cataracts
nephropathy
susceptibility to infections
Goals of insulin therapy
reduce symptoms of diabetes
keep average blood glucose levels below 150mg/dL
prevent/delay onset of complications
What causes diabetic ketoacidosis?
uncontrolled oxidation of fatty acids (accumulation of ketone bodies) (byproduct organic acid)
What functional group in glucose makes it reactive?
aldehyde
What products can glucose be oxidized into?
reactive dicarbonyls
- glyoxal
- methylglyoxal
What is AGE/RAGE
AGE – advanced glycation end products
formed by oxidation products of glucose and proteins that bind irreversibly
results in loss of protein function
RAGE – receptor for advanced glycation end products
Where is RAGE located?
leukocytes and endothelial cells
cell surface proteins
peptides containing CML and CEL (lysine + glucose products) bind to RAGE and promote inflammation
what happens when rage is bound?
inflammation
what is aldose reductase pathway (poly pathway)? where is it located?
occurs in nerves; consumes large amounts of NADPH and causes oxidative damage of neurons
what pathway is aldose reductase in?
polyol pathway
what is the result of polyol pathway?
neuropathy
what/where is hexosamine pathway?
F6P accumulates; causes changes in protein function
What is rate-limiting step of glucose utilization?
fructose-6-phosphate –-> G3P
What happens in the protein kinase C pathway?
Buildup of G3P activates protein kinase C inappropriately
protein modification
