chapter 25 - exam #2

insulin

carrier protein and hormone

no insulin =

nothing for gluc to attach to

glycogenesis

glycogen formation

glycogenolysis

breaking down the bodys stored gluc

gluconeogenesis

making gluc from non-carbs

hypoglycemia

low blood sugar

cause: not eating, stress, too much insulin, too much exercise

patho: when gluc drops…brain and liver detect it and the body will try and raise bs; liver can sustain gluc for 12 hrs unless demand is increased

sx: sweating, hangery, dizzy, irritable, HA, seizures, confusion

*one should eat fast acting carbs is gluc drops

hyperglycemia

bs is too high

DM is the most common cause

sx: polydipsia, polyuria, fatigue, HA

diabetic ketoacidosis (DKA)

body does not have enough insulin and starts breaking down fat for energy which makes ketones

causes: T1DM, not taking insulin as prescribed, alc. use disorder

sx: polydipsia, polyuria, weakness, abdo pain, kassmules aspirations, fruity smelling breath

dx: gluc > 250 and pH is acidic, ketones in blood and urine

tx: IV fluids, IV insulin, potassium replacement (insulin shifts potassium into cells which makes it low)

role of insulin

after eating carbs → gluc enters blood; this high gluc in blood causes the kidneys to release insulin → then insulin will bind to receptors on cells which “opens the door” for gluc to enter cells

gluc is then → used for energy, stored as glycogen in liver and muscles for later use, and if there is extra…its converted into fat

hyperinsulinism

when the body’s cells resist insulin and it will keep being released which causes high insulin in the blood

overtime can lead to T2DM

T1DM

not producing insulin from birth

sx: 3’p - polyuria, polydipsia, polyphagia; wt loss, fatigue, increased infections (candida of genital tract)

in children DKA is the 1st sx

T2DM

pancreas secretes too much insulin at first to try and overcome the resistance but eventually the pancreas gets tired and can’t keep up so blood sugar rises

remember if cells resist insulin, glucose stays in the blood

sx: sedentary life style, hx of HTN, fatigue/low energy, obese, recurrent infections, fasting BS >126

DKA is usually NOT a sx

diagnosing DM

• fasting glucose → > 126 for DM, 100-125 for pre DM

• random plasma glucose → > 200 for DM

• oral gluc tolerance test → pt drinks 75 g of gluc drink and check gluc some hours later; > 200 for DM, 140-199 for pre DM

• A1C → > 6.5 for DM, 5.7 - 6.4 for pre DM

• urine testing → can detect sugar in urine (glucosuria)

• c-peptide test → measures natural insulin production; low/no c-pep = T1DM, high c-pep = T2DM

chronic complications associated w/ DM

eye damage (retinopathy) → can lead to blindness

kidney damage (nephropathy) → can lead to kidney failure

nerve damage (neuropathy) → numbness, pain, or weakness in hands and feet

cardiovascular and PVD

chronic complication occur in DM b/c…

elevated bs overtime can damage blood vessels

can also effect WBCs which causes poor healing and frequent infections

lifestyle changes to tx DM

exercise → contracting muscles do not require insulin for entry into cells to it can lower blood gluc

manage carbs:

1 g of carbs = 4 cals

example question → pt newly dx w/ T2DM is prescribed a diet of 1900 cals a day w/ 50% of cals being from carbs. how many grams of carbs should pt have a day?

50% of 1900 → 1900/2 = 950

since 1 g of carbs = 4 cals … 950/4 = 237.5 g of carbs daily

care for DM

periodic lipid and bp monitoring

pt self-monitoring blood gluc w/ glucometer

insulin therapy, glipizide’s, GLP1s etc.