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diabetes
nursing 241
| Question | Answer |
|---|---|
| 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
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