mattisensept's version from 2017-09-27 20:31

Section 1

Question Answer
goals of diabetic managementreduce symptoms, promote well-being, prevent acute complications, prevent long-term complications, delay long-term complications
how?maintain blood glucose levels, the key is teaching!
collaborative carenutritional therapy, drug therapy (insulin & oral hypoglycemic meds), exercise, self monitoring
insulin storage-rulesheat and freezing alter it, vials in current use can be stored @ room temp for 4 weeks, avoid direct sunlight, extra insulin in fridge, traveling pt (cooler ok)
pre-filled syringes30 days in fridge, if cloudy (pre-filled, stored upright w/needle up), when ready for use --> roll in hands to warm it up and re-suspend the particles before injecting
insulin pumpcontinuous subQ infusion, change site every 2-3 days & delivers rapid or short acting insulin 24/7, check insertion site for redness, disadvantage to increasing BG monitoring (4-6 times a day)
intensive insulin therapy multiple daily injections w/frequent self monitoring of serum glucose, this method has the best change of achieving near normal glucose levels throughout the day, this is more complicated and more likely that patient will have hypoglycemia reaction
oral agentssulfonylureas, meglitinides, biguanides, alpha-glucosidase inhibitors, thiazolidinediones
B andrenergic blockersmask hypoglycemia & prolong the hyooglycemia effects of insulin
thiazide & loop diureticscan potentiate hyperglycemia by inducing potassium loss

Section 2

Question Answer
type 1 DM the planwork with their usual preferences for intake, take into account their exercise pattern
if fixed insuling regimenit is very important to have a routine of time and calories and exercise
if rapid acting or insulin intensive or pumpall allow the client to be more flexible depending on the circumstances, need to know how much more or less to give themselves depending on their meal and exercise
type 2 the planemphasis based on achieving targets for glucose, lipids and BP, calorie & fat reduction, not a "Set in stone" strategy, space meals out, shoot for 5-7% reduction in weight, teach regular exercise, lifestyle changes and monitoring
exercising and eatingshould eat prior because of reduced serum glucose, sustained exercise (take small cab snacks every 30 mins), monitor BG before after and during. Be consistent (too much=stress=cortisol)
physical and emotional stressincreased BG levels--> hyperglycemia
if under ill or stresscontinue regular meal plan (calories are important), increase non-caloric fluids, continue taking meds as perscibed, check BG every 4 hours, sugar >240 (check ketones)
if illness leads to loss of apetitecontinue meds & supplemental food intake w/caloric liquids

Section 3

Question Answer
hypoglycmialow blood sugar <70, confusion, irritability, diaphoresis, tremors, hunger. weakness. visual disturbances, if not treated (loss of consciousness, coma, death)
people who are not awarethose with neuropathy, elderly, B-adrenergic users
if you suspect hypoglycemiaassess the patient, begin assessing for causes of these S&S, give 15-20 gm of simple(fast) sugars, re assess 15 min later
follow up with complex carbs and protein intake (long term)
If it gets worse... administer 25-50 ml of glucose solution IV push, another assessment after, stress to patient when teaching hypoglycemia reaction

Section 4

Question Answer
DKAalso called diabetic acidosis or diabetic coma
what happens?big insulin deficiency, massive hyperglycemia, ketosis, acidosis, dehydration, electrolyte depetion
who is at risk?Mostly type 1 and undiagnosed, can also be type 2, stress, illness, sx, death, divorce, infection
what is happening serum insulin falls and serum sugar rises so cells cannot utilize it, cellular metabolism begins with a by-product of ketones, ketones accumulate in the blood and metabolic acidosis ensues, ketonuria as body gets rid of them, electrolyte depletion (cations are utilized to electronically neutralize the ketones
what is happening cntdinsulin deficiency makes it more likely that protein will degrade and break down (nitrogen tissue loss), insulin deficiency tells the liver to make more glucose (increased hyperglycemia & osmotic diuresis), severe losses of electrolytes, hypovolemia (renal failure and eventually shock), untreated (coma and death)
S&Sdehydration (poor turgoe, dry mucus membrane, tachycardia, orthostatic HTN, skin dry and loose, sunken eyes, abdominal pain, kussmaul respirations
lab values BG >300, pH< 7.30, serum bicarbonate <15, ketones in blood and urine
collaborative care airway & O2, large bore IV access, fluid resuscitation, IV insulin (bolus followed by drip), add dextrose and potassium to IV (sugar and potassium will quickly move into cell, most deaths at this point are form hypokalemia
w/fluid resuscitationassess lung sounds
if acidosis not correctedIV bicarbonate
critical that the nursemake quick assessments, quick and accurate interventions & constantly reassess- changes come quickly
Hyperosmplar hyperglycemia syndrome similar to DKA but not enough insulin so as to not have ketosis, but is life threatening

Section 5

Question Answer
co morbiditiesvisual, lower extremities (neuropathy, weakness), cerebrovascular problems,. kidney
newly diagnosed, ask what do you think it means?important for them to know that it is chronic and serious
serious things to contact providersugar is >300 for 6 hours, check urine for ketones, if ketones see provider, if infection does not show improvement w/in 24 hours, any loss of LOC, sugar does not get >70 even after 3 attempts w/rapid carbohydrates
chronic complicationsdamaged vessels (sugar eats vessels), diabetic retinopathy, nephropathy,neuropathy, integument

Section 6

Question Answer
diabetic retinopathy micro-vascular damage to retina, capillary fluid leaks out and causes damage
prevelence 15 yr diabetic, almost all type 1, most common cause of blindness (20-74)
collaborative careannual dilated eye exams
treatmentphotocoagulation--> coagulation of vessels w/light, cryotherpy(freees the fluid), virectomy (aspirate fluid

Section 7

Question Answer
nephropathy vascular damage to small vessels to glomerulus
prevalence#1 cause of end stage renal disease in US
collaborative carekidney disease significantly reduced w/tight glucose control, HTN contributed, so control it
teachyearly screenings, BP control, serum glucose control

Section 8

Question Answer
neuropathy nerve damage (autonomic & sensory) mostly the peripheral nerves (hands and feet)
prevelance 60-70% have some degree of it
S&S loss of sensation or abnormal sensations, pain & paresthesia
collaborative & teaching controls sugar is the only tx, check feet, watch warm soaks
other neuropathiesautonomic (Gi, sexual function) neurogenic bladder

Section 9

Question Answer
nursing diagnosisineffective therapeutic regimen management, fatigue, risk for infection, powerlessness
goals active patient participation, maintain normal BG levels. prevent chronic complications, lifestyle adjustment w/minimal stress
health promotionidentify those @ risk, routine screen for overweight adults over age 45
collaborative care reduce symptoms, promote well being, prevent acute complications, delay onset and progression of long-term complications
pancreas transplantused for pt w/ type 1 diabetes who have end stage renal disease & who have had or plan to have a kidney transplant, eliminates exogenous insulin

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