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Diabetes
| Question | Answer |
|---|---|
| Incidence Prevalence of type I and type II | 7th leading cause of death in US 20.8 million people or 7% of population 6.2 million people are unaware they have diabetes 90% are type II (often middle age and older adults) 20.9% are age 60 or older Incidence is higher in Men than Women |
| Type I --- Genetic Considerations | HLA-DR and HLA-DQ Most do not develop type I (it is interactive effect of genetic predisp and environmental factors Risk increases with at least one diabetic parent to 1-20/1-50 from general popul of 1-400/1-1000 |
| Type II---Genetic considerations | heredity plays a major role in development offspring of paretns with type 2= 15% chance and 30% chance of having impaired glucose tolerance |
| Type II-- Metabolic syndrome (AKA syndrome X) What is it | simultaneous presence of metabolic factors known to increase risk of develop type 2 and cardio disease |
| Metabolic syndrome--- Abdominal obesiety | Waist circumf is greater than 40 inches (men) Waist circumf is greater than 35 inches (women) |
| Metabolic syndrome--- Hyperglycemia | Fasting glucose level of 100 mg/dL or more OR on drug treatment for hyperglycemia |
| Metabolic syndrome---Hypertension | Systolic BP of 130 mmHg OR disastolic BP of 85 mgHg Or on HTN meds |
| Metabolic syndrome---dyslipidemia | Triglyceride level 150mg/dL Or on drug treatment HDL lower than 40 mg/dL (men)///lower than 50 mg/dL (women) |
| Diabetic Ketoacidosis (DKA)-- Onset | Sudden **More common in type 1 diabetics** mortality rate is 1 to 10% |
| DKA- Precipitating factors | Infection, other stressors, Inadequate insulin dose |
| DKA- Manifestations | Ketosis: Kussmaul respiration, "fruity" breath, nausea, abd pain Dehydration or electrolyte loss: polyuria, polydipsia, weight loss, dry skin, sunken eyes, soft eyeballs, lethargy, coma |
| DKA--Serum glucose | >300 mg/dL Ketones are present in Urine |
| Primary intervention for BOTH DKA and HHNS | administration of fluids and insulin |
| HHNS is more prevalent in... | Older adult clients and individuals with untreated or undiagnosed type 2 DM |
| HHNS serum glucose level | >600 mg/dL |
| HHNS onset/precipitating factors | Gradual/infection, other stressors, poor fluid intake |
| HHNS manifestations | Altered CNS function with neurologic symptoms Dehydration or electrolyte loss (same as with DKA) generalized seizures and reversible paralysis |
| Fluid replacement in HHS | first objective is to increase blood volume. in shock or severe hypotension give normal saline. infuse fluids @ 1 L/hr until BP and urine output are adequate then reduce to 100 to 200 ml/hr |
| Monitor for signs of cerebral edema (during fluid replacement for HHNS) | abrupt changes in mental status, abnormal neurologic signs, coma |
| IV insuline to treat HHNS | initial bolus of 0.15 unit per kg IV followed by drip of 0.1 unit per kg per hour until blood glucose falls to 250 mg/dL reasonable goal is reduction of 50 to 70 mg/dL per hour Monitor for hypokalemia |
| Potential for hypoglycemia | @1 to 5 yrs after diagnosis of type I diab body stops response to hypoglycemia *pancreas loses ability to secrete glucagon in response to hypogly *response to epinephrine is also decreased hypogly unawareness-- no longer have warning signs (30 yrs ^ |
| symptoms of hypoglycemia neuroglycopenic | (brain glucose GRADUALLY declines) warmth, weakness, fatigue, difficulty thinking, confusion, behavior changes, emotional lability, seizures, loss of consciousness, brain damage, death |
| sympt of hypoglycemia neurogenic | (ANS triggered by RAPID decline) Adrenergic (Shaky/tremulous, heart pounding, nervous, anxious) Cholinergic (sweating, hungry, tingling) |
| Hypoglycemia Management | Identify patient @ risk Monitor blood glucose levels Monitor for signs ofof hypoglycemia Provide simple carb Provide complex carb and protein Administer glucagon Contact Emerg srvs Admins IV glucose Maintain IV access Maintan patent airway |
| Hypoglycemia management (cont...) | Protect from injury review events prior to determine cause |
| Hyperglycemia Management | 1. Assess airway, LOC, hydration status, electrolytes, blood glucose level 2. check BP, P, Resp, every 15 min until stable 3. record urine output, temp, mental stat every hr 4. after treatment and pt is stable monitor vitals every 4 hrs |
| Hyperinsulinemia | Chronic high blood insulin levels *can occur w/ intensive tx schedule & may result in weight gain *may need to manage hyperglycemia with decrease in calories rather than increase in insulin |
| Macovascular complications Cardiovascular disease | *most common complication @ higher risk of MI (higer for women) 50% of diabetics have CVD @ diagnosis renal disease increases the risk of coronary heart disase and death from MI ADA recom BP less than 130/80 mmHg and LDL less than 100 mg/dL |
| Macrovasular comp Cerebrovascular disease | diabetes damages cerebrovascular arterial circulation *elevated blood glucose levels @ the time of stroke may lead to greater brain injury and higher mortality |
| Microvascular Complications Eye and vision comp | 25 X more common in pts with diabetes r/t duration of disease after 20 yrs nearly all pts with type I have some degree of retinopathy r/t problems that block retinal blood vessels and cause them to leak |
| nonproliferative diabetic retinopathy | causes structual problems in the retinal blood vessels BUT growth of new blood vessels is not stimulated areas of poor circulation, edema, hard fatty deposits in the eye and retinal hemorrahges microaneurysms->leak fluid & blood in retina>retinal edema |
| Proliferative diabetic retinopathy (PDR) | when retinal blood flow is poor and hypoxia develops retinal cells secrete "growth factor" which = new blood vessles in the eye that are thin and fragile and bleed easily = eye hemorrhage = more vision loss *fasting blood glu ^ 129 mg/dL |
| Renal disease risk factors | 10 to 15 yr hx of DM, DM retinopathy, poor blood glucose control, uncontoll htn, genetic predisposition |
| Renal disease earliest clinical sigh | microalbuminuria--- testing for pts that have had type 1 for @ least 5 yrs and in ALL pts with type 2 |
| Cause of Renal disease | chronic high blood glucose levels cause HTN in kidney blood vessels and excess kidney perfusion which damages kidney (blood vessles become leakier esp in glomerulus) filtration of albumin = deposits in kidney tissue= narrow vessels= < O2= hypoxia/death |
| Renal disease drug therapy | ACE inhibitors decrease levels of albuminuria and the rate of progression of kidney disease |
| Renal disase nutrition therapy | restrict protein to 0.8g/kg of body weight |
| Fluid management/elect management with renal disease | can help prevent more loss of kidney function-- avoid dehydration (overuse of diuretics) teach pt to report edema or orth hypo dosage of insulin needs to be adjusted when pt starts dialysis |
| Nutrition Principles for protein | 15% to 20% of calories if pt has microalbum decrease to 10% |
| Nutrition (Carbs) | 45% to 65%/// 130 g carb/day carbs from fruit, veg, whole grains, legumes, and low fat milk |
| nutrition (fat/cholesterol) | Less than 7% of total calories decrease intake of trans fat cholesterol < 200 mg/day 2 or more servings of fish/week |
| Fiber | 14g per 1000 calories (1st goal) ADA-- 25g/day legumes, fiber rich cereal, fruits vegs |
| sweeteners | FDA has approved 5- |
| alcohol | two beverages for men and one for women to avoid alcohol induced hypogly-- ingest w/ or shortly after meals one bev is subs for 2 fat exchanges |
| Exchange System | based on carbs, meat/meat substitutes, fat |
| Carb counting (CHO) | b/c fat and protein have little effect on after meal blood glucose levels uses total grams of carbs regardless of food source *1 unit of rapid acting insulin for 15 g of carbs* |
| Mixing insulins | Insulin glargine (lantus) should not be mixed b/c of low pH of its diluent NPH and short acting can be mixed and used immediately or stored Rapid acting can be mixed with NPH rapid w/ intermediate should be inject 15 min before meal |
| Complications of insulin therapy lipohypertrophy | incrased swelling of fat that occurs @ the site of repeated insulin injections |
| Dawn phenomenon | nightime release of growth hormone that causes blood glucose elevattions @ 5am to 6am --provide more insulin @ night |
| Somogyi phenomenon | morning hypoglycemia from counteregulatory response to nighttime hypoglycemia --ensure adequate dietary itake @ bedtime |
| Rapid Acting Insulin | insulin aspart (Novolog) onset 0.25 hr/peak 1-3 hr/dur: 3-5hr insulin glulisine (Apidra) onset:0.3hr/peak:0.5-1.5hr/dur:3-4hr Human lispro inj (Humalog) onset 0.25 hr/peak 0.5-1.5hr/dur:5 HRS |
| Short Acting Insulin | Regular (Humulin R, Novolin R, ReliOn R) onset: 0.5 hr/peak 2-5 hr/dur 5-8 hr Humulin R (Concentrated U-500) onset:1-5 hrs peak 4-12 DURATION 24 hrs |
| Intermediate Acting | NPH (Humulin N, Novolin N, ReliOn N) onset 1-5 hr/peak 4-12/dur 16-24+ Insulin determir (Levemir)-DO NOT MIX!! onset: 1 hr, peak 4-12, dur 5.7-24 hrs |
| Mixtures of Reg and rapid | Most are 70/30 with rapid acting being the smaller amount |
| Long Acting | insulin glargine (Lantus) onset 2-4, peak NONE, duration 24 hours DO NOT MIX!!! |
| Insulin regimens | duplicate normal insulin release patterns usual starting dose is b/t 0.5 and 1 unit/kg of body weight/day continuous insulin is 40-50% remainder is premeal dose of rapid acting test glucose 1 to 2 hrs after meals and w/i 10 min of next meal |
| Factors influences insulin absorp | site, type, dose, physical activity site--fastest in abdomen followed by deltoid, thigh and butt factors that increase blood flow such as heat massage, excersie increase absorption |
| 2nd gen sulfonylureas action | increase insulin section in type 2 DM |
| 2nd gen sulfonylureas SE | weight gain, hypoglycemia underweight older pts w/ cardiovas, liver or kidney disease are more at risk for hypoglycemia |
| 2nd gen sulfonylureas teaching | take 30 min before meals how to prevent/treat hypoglycemia |
| 2nd gen sulfonylureas examples | Glipizide (Glucotrol)/Glimepiride (Amaryl) |
| 2nd gen sulfonylureas drug reactions (lead to hyperglycemia) | Adrenalin Calcium channel blocking agens Corticosteroids Estrogen Lasix INH Dilantin Rifampin Thiazide diuretics |
| 2nd gen sulfonylureas drug reactions that lead to hypoglycemia | ACE Alcohol Analgesics Beta Adrenergic blocking Heparin H2 antagonists MAOIS NSAIDS Sulfonamides Tricyclic Antidepressants |
| Meglitinide analogues action | increase insulin section in type 2 diabetics |
| meglitinide analogues SE | simular to sulfonylureas |
| meglitinide teaching | take 1-30 min before meals omit when skipping meals add dose if extra meal is eaten |
| meglitinide examples | Prandin (repaglinide) |
| Biguanides Action | lowers both basal and post meal glucose levels in pts w/ type 2 diab by reducing hepatic glucose production and tissue sensitivity to insulin |
| Biguanides SE: | ** does NOT cause weight gain or hypoglycemia**abdominal pain, diarrhea, monitor for lactic acidosis, liver and renal impairment |
| Biguanides teaching | take w/ food monitor liver and renal function monitor cardiopulmonary status Monitor 4 lactic acidosis (fatigue, muscle pain, diff breath, abd pain, dizziness, light head, irreg heart beats) *contr.in pts with renal disease, liver, etoh ab, chf, ^80y |
| Biguanides Example | Glucophage (Metformin) 1st used |
| Thiazolidiones action | Improve insulin sensitivity & decrease liver glucose production Increase insulin action in muscle, fat, and liver tissue |
| Thiazolidiones SE: | Increase in adipose tissue, fluid retention edema w/ dev of CHF, infection, h/a, liver damage |
| Thiazolidiones Teaching: | need liver funtion tests, report n/v, abd pain, fatigue, anorexia, dark urine Advise women to need for effective contraceptive |
| Thiazolidiones Example | pioglitazone (Actose) |
| HbA1C and mean plasma glucose level | the higher the glood glucose level is over time the more glycoslyated hemoglobin becomes. tests shows avg blood glucose levesl during prev 120 days (life span of red blood cell) |
| Continuous subcut infusion (CSII) | increase in insulin @ mealtime if meal is skipped does is not given can lead to ketoacidosis **test ketones when glucose is ^ 300 mg/dL |
| Cultural awareness | High risk for Af Am, Am Indians, Mex amer HTN in diab pts is at least 2 X higher than nondiabetics (esp in whites and af amer) microvascular comp of eyes, nerves, kidneys are more common in afr am & indians (lack of health care, lifestyle issues etc) |
| Diagnosis of Diabetes Fasting plasma glucose | NPO 8 hrs, pred medication, 2 seperate results ^ 126 mg/dL *** preferred test in non preg** |
| Oral glucose tolerance test | non routinely used> inconveinent, $$$, time consuming used to diag gestational diab **eat bal diet w/ carb intake of @ least 150g for 3 days prior *Carb rest, bedrest, illness, drugs (phenytoin, diuretics, nicotinic acid glucocoricoids affect results |
| oral glucose tolerance test cont... | *Test performed in morning after 10-12 hr fast *Fasting sample obtained *drink 300 mL of bev 5 min before of sample *blood samples drawn at 30 min intervals for 2 hrs *during test you will remain @ rest and can not smoke or drink liquids |
| Diabetic neuropathy | damage to sensory nerves= pain or loss of sensations damage to motor nerve fibers= muscle weakness autonomic nerves=dysfunction in every part of body hyperglycemia= blood vessel changes that cause nerve hypoxia |
| Diabetic neuropathy --prevention of high risk conditions | keep blood glucose levels in the normal range stop smoking |
| Foot Risk Categories Risk Category 0 | *has disease that leads to insensitivity *has protective sensation *has not had a plantar ulcer |
| risk category 1 | *does not have protective sensation *has not had a plantar ulcer *does not have a food deformity |
| risk category 2 | *does not have protective sensation *has not had a plantar ulcer *does have a foot deformity |
| risk category 3 | *does not have a protective sensation *has history of plantar ulcer |
| Management category 0 | *examine feet at each visit, at least 4 x per year *foot clinic visit once a year *patient education |
| Management category 1 | *examine feet @ each visit at least 4 x yr *foot clinic visit every 6 months *soft insoles *patient ed |
| Mangeement category 2 | *examine feet @ each visit 4x yr *foot clinic visit every 3-4 months *custom-molded insoles *prescription footwear *Patient ed |
| Management category 3 | *examine feet at each visit 4 x yr *foot clinic visit every 1-2 months *custom-molded insoles *Rx footwear *patient ed |
| The diabetic foot Assess the patient for risks of diab foot prob | -hx of prev ulcer -hx of prev amputation |
| diab foot Assess the foot for abnormal skin and nail cond | -dry, cracked, fissured skin -ulcers -toenails; thickened long nails ingrown nails -tinea pedis; onychomycosis (mycotic nails) |
| diab foot assess for status of circulation | -symptoms of claudication -presense of absence of dorsalis pedis or post tibial pulse -prolonged cap refil (greater than 25 sec) -presence or absence of hair growth on the top of the foot |
| diab foot assess for evidence of deformity | -calluses, corns -prominent metarsal heads -toe contractures; clawed toes; hammertoes -hallux valgus or bunions -charcot foot (rocker bottom) |
| diab foot assess for loos of strenght | -limited ankle joint ROM -limited motion of great toe |
| diab foot assess for loss of protective sensation | -numbness, burning, tingling -semmes-weinstein monofilament testing at 10 points on each foot |
Created by:
strangesangria
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