kania pt 0 Flashcards
hyperglycemia
results from defects in insulin secretion, resistance to insulin action, or both
autoimmune destruction of beta cells
leads to insulin deficiency and/or resistance to insulin
effects of long-term hyperglycemia
leads to organ damage in eyes, kidneys, nerves, heart, and blood vessels
signs and symptoms of hyperglycemia
relate to alterations in carbohydrates, fat, and protein metabolism
function of insulin and counterregulatory hormones
regulation of carbohydrate and fatty acid metabolism
organs involvement in glucose homeostasis
brain –> insulin dependent
fat/muscle tissue –> insulin dependent
liver –> plasma glucose levels with increased production; production decreases with rise of insulin
increase in insulin means
decrease glucose production by liver
decreased glycogenolysis and gluconeogenesis
stimulate tissue glucose uptake
suppress FFA release from fat cells
egregious eleven (ominous octet)
1) beta cells may be destroyed or simply quit working (leads to decrease insulin)
2) decreased incretin effect
3) dysfunction of a cell leads to increase glucagon levels
4) adipose insulin resistance leads to increased lipolysis
5) muscle insulin resistance leads to decrease peripheral muscle uptake (not using glucose adequately)
6) liver insulin resistance leads to increase glucose production (cannot recognize glucagon)
7) changes of hormones in the brain –> increased appetite, decreased morning dopamine surge, increased sympathetic tone
8) different gut bacteria can modify blood glucose levels and may decrease GLP-1 levels
9) beta cell destruction via autoimmune reactions or increased inflammation
10) quick stomaching empty –> increased glucose absorption
11) up regulation of SGLT2 –> increased glucose reabsorption in kidney
why do many older adults not get diagnosed with T2DM despite having clinical presentation?
common symptoms (polyuria, nocturia, etc) are associated with old age
pt just assume that is the cause not T2DM
metabolic syndrome
HTN
obesity
dyslipidemia (high TG and low HDL)
drugs that increase hepatic glucose output
glucocorticoids
sympathomimetics
niacin (with higher doses only)
drugs that decrease insulin secretion
phenytoin
beta blockers
calcium channel blockers (can lead to proteinuria)
immunosuppressants
B-block usage
able to use, but consider the indication and if its necessary
caution use in brittle diabetics especially with ultra short-acting agents
can mask the signs and sx of acute hypoglycemia
A1C criteria for diabetics
greater or equal to 6.5%
patients with high red blood cell turnover (like in sickle cell anemia or pregnancy) do not have to have this for diangosis
treatment for IFG, IGT, or increased risk for diabetes
need monitoring
consider pre diabetic drug therapy, but definitely lifestyle changes