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nursing 241

insulin makes glucose into _____ glycogen
where does glycogen reside? muscle and liver
in a normal person what does the body do when blood sugar starts to get low? glucagon goes into liver and breaks down glycogen into sugar
what is glyconeogensis? when glucagon goes into liver and breaks down glycogen into sugar
what is gluconeogenosis? gluconeogensis occurs when there is no glycogen left to break down so fat and protein make new glucose for the body
is glucose intracellular or intravascular? intracellular
what are the 3 P's of type 1 diabetes? polydypsia, polyuria, polyphagia
what do type 2 diabetics commonly suffer from that raises the blood sugar? pancreatic exhaustion due to the pancreas compensating for so long
why don't type 2 diabetics get DKA? in type 2, fat isn't broken down. therefore type 2's don't experience gi symptoms
symptoms of type 2 hyperglycemia, hyperosmolar, nonketotic, coma/syndrome - used to describe a type 2 who'se blood sugar is off the charts
diagnostic criteria random blood sugar draw >200. fasting blood sugar >126. oral glucose tolerance test. hgb a1c >6.5%. KETONES ARE NOT DIAGNOSTIC CRITERIA B/C THEY CAN BE PRESENT AT OTHER TIMES SUCH AS STARVATION
ppl at risk for diabetes family members w/ DM, obesity, over 45, steroids, BP >140/90, HDL <35, tri's >250, hx of gestational diabetes, baby over 8lbs 13oz., sedentary lifestyle, impaired glucose tolerance, impaired fasting glucose
which are modifiable? exercise and diet, meds
factors of type 1 insulin deficiency, usually discovered under 30, abrupt onset, idiopathic, b cell destruction, usually nonobese, diabetes diet=mandatory, prone to ketones at onset or during insulin deficiency. NO ORAL HYPOGLYCEMICS
factors for type 2 usually above 35, insidious onset,dysfunction b cell or obesity/nutrition, c-peptide low normal or high, obese, insulin not required for every pt, oral hypoglycemics, resistant to ketones insulin resistant, insulin deficiency, defective insulin secretion
what is diabetic ketoacidosis? seen in type 1 diabetics. when there isn't enough insulin, body starts feeding off of fat for glucose. the breakdown of fats releases ketones in the body, which is acidic leading to DKA - pt experiences abd discomfort
what causes dka? decreased insulin or missed dose of insulin, illness or infection bc they are stressors, undiagnosed or untreated diabetes
hx you will see on pt chart n/v, abd pain, polyuria w ketones, changes in loc
physical s/sx for dka kusmalls resp, juicy fruit breath, dehydration which can lead to cardiac arrythmias, glucosuria, low bicarb
main difference between hhnk and dka KUSMALLS RESP
what is the mainstay treatment for dka fluids bc the pt's are so dehydrated. also may have insulin drip. these pt's have inc BS and they're acidotic. BS usually corrects before acidosis. may see order for d5 to replace insulin drip
hhnk symptoms dehydration, bs 600-1200, hypotension, inc risk for mi and stoke r/t atherosclerosis, inc osmolarity, inc bun/creatinine
treatment for hhnk iv fluids w insulin drip, k replacement of hypokalemic. once bs corrects, switch to d5
long term complications of diabetes retinopathy, nephropathy, neuropathy, coronary disease, cerebral vascular disease, peripheral vascular, hypertension, infection
factors that increase blood sugar food, stress, meds, menses (estrogen)
factors that decrease blood sugar insulin, oral hypoglycemics, exercise, etoh
treating exercise induced hypoglycemia stop exercising, ingest 15g of carbs, monitor bs q15mins til at least 80. if bs is still <80 repeat snack and monitor q15mins again **if bs <100 before exercise=snack
biguanide - metformin excreted by kidneys. need kft and lft. dec intestinal absorption. d/c 48 hrs before using contrast and wait 48 hrs after contrast. interferes w anticoag, corticosteroids, diuretics
thiazolidinediones - Avandia inc insulin sensitivity. dec tri's and hdl. may inc risk of hf and mi. imp for lft's bc it's metabolized in liver.
sulfonylureas - glyburide, glipizide, glimpiride stimulates pancreas to release insulin - may expedite need for insulin therapy
meglitinides - prandin, starlix inc insulin release postprandially. use caution w liver impairment. must take w meals!
alphaglucosidase inhibitors metabolized by intestinal bacteria and digestive enzymes. works by delaying carb absorption. best for those w normal fasting bs and inc after meals. prevents absorption of glucose, need glucose tablets. s/e: GAS!
what type of insulin can be in a drip? short acting - regular insulin
what type of insulin is lantus? long-acting. mimicks baseline. never mix lantus with anything. should be taken once a day and at the same time every day
complications of insulin therapy local allergic rxns, lipodystrophy, lipohypertrophy,
Created by: eileenrx