Diabetes Mellitus Study Guide

DIABETES MELLITUS * Chronic multisystem dz , abnormal insulin production / spoiled utilization * Disorder of glucose metamorphosis related to absent/ insuff insulin bring or poor utilization of inslin thats available * 7th leading pay off of dying * leading private road of blindness, ESRD, lower limb amputation * contri entirelying ingredient for heart dz/ stroke stake 2-4 x gameer than without DM * INSULIN ductless gland produced by cells in islets of Langerhans of pancreas.Normal continously into telephone circuitstream ( basal rate), or increased w/ meals (bolus) * Normal glucose range 70-120 mg/dL, average insulin secreted day-by-day 40-50 U 0. 6 U/kg * Glucagon, epinephrin, GH, cortisol oppose effects of insulin counterregulatory hormones they rent glucose lebels, get chthonian ones skin glucose production by liver-colored, movement of glucose into cells. Insulin released from cells as precursor / proinsulin thru liver enzymes realize insulin &038 C-peptide ( C-peptide in serum &038 urine indicator of cell function) * in germ plasm insulin subsequently meal storage of glucose as glycogen in liver/ muscle, isoniazidibits gluconeogenesis, plummet de carriage, protein synthesis * Nl over iniquity fasting release of stored gucose from liver, protein from muscle, fat from adipose create from raw material * Skeletal muscle &038 adipose tissue receptors for insulin insulin-dependent tissues reference I Diabetes Juvenile infringement, insulin-dependent, s/s abrupt but dz suffice present for several yrs, 5-10%, absent or momentimal insulin production, computer virus/toxins, under 40, 40% before 20 yr * s/s thirst( polydipsia), polyuria, polyphagia ( hunger), fatigue, wt bolshie, Kussmaul respirations * tolerant mediated dz T-cells attack &038 destroy cells * genetic predisposition &038 exposure to virus * Idiopathic diabetes not atoimmune, strongly isoniaziderited, in small pt w/ type I DM , Afri hatful/Asian * Predisposition HLAs tender leukocyte ntigens when exposed to viral transmission cells destroyed * commodious preclinical period, s/s develop when pancreas can no longer produce competent insulin to maintain nl glucose takes * Req. insulin from outside source exogenous insulin eg. enterion * No insulin diabetic ketoacidosis (DKA) life threatening, results in metabolous acidosis * honeymoon period newely diagnosed pts, tx initiated pt experience remissions req little insulin because cells produce suff amount of insulin lasts 3-12 mths then req permanent insulin Prediabetes * attemptiness for develop diabetes glucose take aims high but not high enough for diabetes diagnosis * impaired fasting glucose IGF 100-125 mg/dL * 2 hr ad-lib exam glucose security deposit test OGTT 140-199 mg/dL * HgB A1C 5. 7%-6. 4% take a chance for diabetes * Increased jeopardize for evolution DM type II if no interdictive measures develop DM in 10 yrs * Long circumstance damage to organic structure heart, phone line vessels occur in prediabetes * Usually no symptoms * Maintain healthy weight, consumption incessantly, healthy diet take chances of developing diabetes persona II Diabetes * Adult onset, non-insulin dependent, 90% * > 35, overweight, tendency to run n families * African Am, Asian, Hispanics, Amerian Indians Some insulin is produced but either insufficient for body inevitably / poorly utilized * Gradual onset, many yrs undetected hyperglycemia, 500- universal gravitational constantmg/dL * advance(prenominal) usu. asymptomatic high risk pt screen each year * Fatigue, recurrent inf, vaginal yeast inf, candida inf, procrastinateed wound healing, visual changes * Risk factor obesity ( abdominal/ visceral ) * 4 major metabolic abnormalities * insulin defense > tissue no rejoinder to insulin / unresp receptors receptors argon located on gaunt muscles, fat &038 liver * ability of pancreas to produce insulin fatigued from compensatory prod of insulin, ell volt aic pile lost * inappropriate glucose by liver too much glucose for body take ons type II * altered prod. of hormones &038 cytokines by adipose tissue ( adipokines) role in glucose &038 fat metabolism type II. Two adipokines ( adiponectin &038 leptin ) displace insulin sensitivity altered mechanism in type I &038 I * Metabolic syndrome > risk for type II &038 cardio dz, cluster of abnormalities, insulin resistance, insulin levels, triglycerides, HDLs, LDLs, HTN * Risk factors for metabolic syndrome central obesity, sedentary lifestyle, urbanization, westernization Gestational Diabetes During pregnancy, 7% of pregnancies * High risk flagitious obesity, prior hx of gestational DM, glycosuria, polycystic ovary syndrome, family hx of DM II screened at 1st antepartum visit * Average risk OGTT at 24-28 wks of gestation * Higher risk of cesarean delivery, perinatal death, neonatal complications * Will have nl glucose levels within 6 wks canpartum but risk of DM II in 5-10 yrs * nutritional therapy 1st line , if doesnt work insulin therapy Other specific types of diabetes * delinquent to other medical condition or treatment causes abn blood glucose levels * injure , injury, destruction of cell function Cushings, hyperthyroidism, pancreatitis, cystic fibrosis, hemochromatosis, TPN * Meds > corticosteroid (prednisone), thiazides, phenytoin(Dilantin), antipsychotics clozapine * Tx underlying condition, stop meds Diagnostic studies * A1C > 6. 5 % great convenience, no fasting req, less day to day alterations during focussing/ illness * FPG >126 no thermal intake for 8 hrs prior interrogatory confirmed by repeat testing other day if has s/s and FPG>126 further testing OGTT not req * 2 hr OGTT >200, glucose load 75g accuracy depends on pt preparation, and factors that influence results.False negative > impaired GI dousing, falsely elevated> onerous restrictions of carbs, discerning illness, meds corticosteroids, contraceptives, bed r est * IFG impaired fasting glucose &038 IGT > prediabetes, 100-125 mg/dL, IGT 2 hr > 140-199 * Glycosylated HgB HgB A1C > amount of glucose attached to HgB molecules over lifespan ( RBC 90-120 years ) DM pts should soften it habituely, arrogatee to monitor success of tx / make changes to tx < 6. % risk of retinopathy, kidney disease, neuropathy dz affecting RBCs can affect A1C results Treatment * Goals > s/s, promote strong being, prevent acute complications, prevent/ hinder onset/ forward motion met when pt maintain glucose level as near to nl, daily decisions about food for thought intake, blood glucose testing meds, exercise * Rapid acting insulin lispro (Humalog), aspart (NovoLog) onset 0-15 min, tallness 60-90 min, dur. -4 hrs , clear, give 15 min before meals bolus * Short acting languid (Humulin R, Novolin R) onste ? -1 hr, stature 2-3hr, dur 3-6 hrs, injected 30-45 min before meals bolus * Intermediate acting NPH, basal insulin, onset 2-4hrs, peak 4-10hrs can result in hypoglycaemia, dur. 10-16 hrs, can be tangled w/ short &038 fast, cloudy, must be agitated before adm. Long acting glargine (Lantus), detemir ( Levemir) addition to meal clip insulin, type I, to control glucose between meals &038 overnight, without it risk of developing DKA, no peak risk of hypoglycemia , not diluted or intricate, clear onset 1-2 hrs, dur. 24hrs +, basal * Combination > pt dont want 2 separate injections, 2 type of insulin mixed together, not same control of glucose levels as with basal-bolus ahort/ fast mixed w/ ntermediate cater both mealtime &038 basal coverage * Storage > vials room temperature 4 wks, set off &038 freezing alter insulin, between 32-86 F annul direct exp to sunlight, otiose insulin in fridge/ traveling-thermos, Prefilled syringes sight impaired, manual dexterity syringes w/ cudy solution in vertical position needle up to avoid clumping of suspension, rolled gently, warm before injection. * Injection > a bdomen fastest absorption arm, thigh, buttock, rotate within 1 particular order never into site thats about to be exercised (heat = absorption &038 onset), vial 1ml=100U, SQ 90 degrees * Needles ? 5/16 inch (short children, thin adults) gauges 28,29,30,31 higher gauge = smaller diam = more comfortable injection * Recapping done except by soul using syringe, never recap syringe used by pt alcohol swabs in health care facility before inj to HAI, at home soap &038 water * Insulin pump continuous subq insulin infusion 24 hr/d basal rate , loaded w/ rapid acting insulin via plastic tubing to catheter in subq tissue.At meal time bolus . (+) roiled glucose control, standardized to nl physiologic pattern, nl lifestyle, more flexibility (-) infection at site, risk of DKA, cost Problems w/ insulin therapy * Hypoglycemia * Allergic rxn itching, erythema, burning around inj. site, whitethorn improve w/ low dose antihistamine rxns to Zinc, protamine, latex , rubber stoppers on vials * Lipodystrophy atrophy of subq tissue if same inj site used Somogyi effect cringe effect, overdose of insulin induces undetected hypoglycemia in hrs of sleep, produces glucose decline in response to too much insulin s/s headaches, night sweats, nightmares if in first light glucose adcised to check glucose levels at 2-4am if hypoglycemia present at that time.If it is insulin dosage in affecting morning blood glucose is reduced TX less insulin * Dawn phenomenon hyperglycemia on awakening in the morning due to release counterregulatory hormones in predawn hrs ( possibly GH/cortisol) adolescence/ young TX adjustment in timing of insulin adm. or in insulin. Predawn fasting glucose levels insulin production from pancreas , s. ff > wt gain, hypoglycemia * Meglitinides repaglinide(Prandin) insulin prod, less likely cause hypoglycemia because more rapidly absorbed/eliminated, cause wt gain, take 30 min before meal, not if skipped * Biguanides Metformin > glucose lowering, first choice DM II/prediabetes, obese &038 starch blockers slow down carbs absorption, taken with first flake, effectiveness> check 2 hr postprandial glucose levels * Thiazolidinediones Avandia > insulin sensitizers, for pts w/ insulin resistance, dont insulin Production, not cause hypoglycemia risk of MI, stroke , not for pt w/ HF * DPP4 inhibitor Januvia > new class, slow inactivation of incretin hormones DDP4 inh are glucose dependent = risk of hypoglycemia, no wt gain * Incretin mimetics exenatide (Byetta) > stimulate incretin horm which are in DM II, stim. of insulin, Suppress glucagon, satiety = caloric intake, slows gastric change prefilled pen * Amylin analog > Amylin hormone secreted by cells, co secreted w/ insulin Pramlintide (Symlin) is synthetic substance , type I &038 II when glucose level not achieved w/ insulin at mealtimes , subq thigh or abdomen NOT arm , not mixed w/ insulin cause severe hypoglycemia * blockers &8212 masks s/s of hypoglycemia, prolong hypoglycemic effects of insulin * Thiazide / loop diuretic &8212 hyperglycemia, K Nutrition Type I > meal en mucklening, exercise, developed w/ pts alimentation habits &038 legal action pattern in mind, day to day consistency in timing &038 amount of food eaten * Type II > wt privation = change insulin resistance, total fats &038 simple sugars = calorie &038 carbs intake Spacing meals , wt loss 5-7% = glycemic control, regular exercise * Carbohydrates > sugar, starches, fiber whole grains, fruits, veggies, low fat take out include min 130g/d * Glycemic index GI > describe blood glucose levels 2 hrs after(prenominal) carb meal , GI of 100 = 50g glucose * Fiber intake 14g/1000 kcal * Fats 7% of total calories , < 200mg/d cholesterol &038 trans fats * Protein same for diabetes / normal nephritic function / gen. population, high proein diet not recommended * Alcohol > inhibits gluconeogenesis ( breakdown of glycogenglucose) by liver severe hypoglycemia in pt on insuli n / oral hypoglycemic dx.Moderate alcohol consumption < 2 drinks men, track carbs w/ separately meal &038 daily, set limit for max amount ( depends on age, wt, activity level) usu. 45-60g /meal also My Pyramid &038 plate method ( ? nonstarchy veggies, ? starch, ? protein, nonfat milk &038 fruit * Exercise > 150 min/wk moderate intensity aerophilous DM II resistance training 3 x wk, virtually adults should 30 min moderate intensity activity 5 x or so days * Exercise > insulin resistance, blood glucose, wt loss which insulin resistance ( may need less meds), triglycerides, LDL, HDL, BP, circulation * Start slowly w/ progression. Insulin, sulfonylureas, meglitinides >risk of hypoglycemia with increase physical activity esp if exercise at peak of dx or no food intake.Effect may last 48 hrs post exercise Exercise 1 hr after meal, have 10-15g carb eat every 30 min. during exercise (prevent hypoglycemia). Before exercise glucose immediate selective information about glucose levels can make adjustments diet, activity, meds * Recomm. for all insulin-treated pts * Multiple insulin injections 3 or more x day, done before meals, before &038 after exercise esp in type I, whenever hypoglycemia suspected, when ill (stress), 2 hrs after become of meal if effective Pancreas transplantation * For pt w/ ESRD, plan to have kidney transplant * Pancreas transplanted following kidney transplant, pancreas alone rare * Pancreas alone only if hx of severe metabolic complications, emotional roblems w/ exogenous insulin, failure of insulin-based centering * Improve quality of life, no exogenous insulin need, no dietary restrictions * scarce partially able to reverse renal &038 neurologic complications * Need long immunosuppression to prevent rejection * Pancreatic islet cell transplantation in observational stage, islets from deceased pancreas via catheter into abdomen portal vein Nursing management * Pt active participant in management of diabetes regimen * Few/no episodes of acute hyper/hypoglycemic episodes, maintain glucose level near nl * Prevent/ delay inveterate complications * Adjust lifestyle to accommodate DM regimen w/ min. stress Nursing assessment Past hx mumps, rubella, viral inf, recent trauma, stress, pregnancy, baby>9lbs, Cushing, acromegaly, family hx of DM * Meds > compliance w/ insulin, OA corticosteroids, phenytoin, diuretics * Eyes > drop eyeballs, vitreal hemorrhages, cataract * Skin > dry, warm, inelastic, pigmented lesions on legs, ulcers(feet), loss of hair on toes * Respiratory > Kussmaul rapid, deep * Cardio > hypotension, weak rapid pulse * GI > dry mouth, vomiting, fruity breath * Neuro > altered reflexes, restlessness, confusion, stupor * MS > muscle wasting * Also electrolyte abnormalities, fasting glucose level >126, tolerance test> 200, leukocytosis, BUN, creatinine, triglycerides, cholesterol, LDL, HDL, A1C 45yrs without risk factors for diabetes Acute intervention * Hypoglycemia, DK A, HHS hypersmolar hyperglycemic syndrome * Stress f acute illness/ surgery > counterregulatory hormones > hyperglycemia ( even minor upper resp infection or flu can cause this) * Continue regular diet, noncaloric fluids (broth, water, diet gelatin, decaffeinated), take OA/insulin as prescribed, monitor glucose Q4H * Acutely ill DM I , glucose>240 test urine for ketones Q3-4H , medium/large report to MD * Ill > eat than normal > continue OA meds/ insulin as prescribed + bread containing fluids (soup, juices, decaffeinated) * Unable to prevail fluids/ food down MD * Dont stop insulin when ill counterregulatory mechanisms will glucose level * Food intake heavy body needs extra energy to deal w/ stress Extra insulin may be needed to meet this demand, prevent DKA in DM I * Intraoperative > IV fluids &038 insulin before, during, after sx when theres no oral intake In DM II w/ OA pardon its temporary measure, doesnt mean worsening of DM * If personal line of credit med ium (w/iodine) > Metformin discontinued 1-2 days before sx, resumed 48 hrs after sx risk of acute renal failure.Resume after kidney function nl ( creatinine checked &038 is nl) * Insulin adm > school proper administration, adjustments, side effects, assess response to insulin tx, if new to insulin assess ability to manage tx safely, cognitive status, ability to recognize/ tx hypoglycemia, if cognitive skill another responsible person must be assigned diff to self inject/ afraid of needles * Follow ups > inspect injection sites ( lipodystrophy ) * Short term warehousing deficit > OA or short acting OA cuz doesnt cause hypoglycemia * OA w/ diet &038 activity, not take extra pill when overindulge * Diligent skin care &038 dental > aily brushing/ flossing, inform dental practitioner about DM * Foot care scrapes, burns treated immediately &038 monitored > nonirritating antiseptic ointment > dry sterile pad> not start to heal in 24 hrs or infection > MD * fix eye e xams * Travel sedentary > walk Q2H to prevent DVT &038 prevent glucose , assoil snacks, extra insulin COMPLICATIONS Diabetic Ketoacidosis DKA * Diabetic coma Profound deficiency of insulin > hyperglycemia, ketosis, acidosis, dehydration * Most likely in DM I pts, but sometimes in DM II ( severe illness/ stress) * Causes > illness, infection, undiagnosed DM I, inadeq insulin dosage, poor self management, neglect * Insulin glucose cant be mightily used for energy fat broken for fuel ketones (by product) serious when ebullient in blood alter pH, cause metabolic acidosis ketonuria (in urine) &038 electrolyes humiliated impaired protein synthesis, nitrogen lost from tissues * Untreated depletion of Na, K, Cl, Mg, phosphate hypovolemiarenal failure/ guardianship of ketones &038 glucose shockcoma (result of dehydration, lytes &038 acidosis)death * s/s > dehydration, poor turgor, dry mm, HR, orthostatic hypotension, Kussmaul , abdominal pain, sunken eyeballs, acetone fruity odor, early s/s > lethargy,weakness * blood glucose >250, arterial blood pH IV access begin fluid/ electrolyte transposition NaCL 0. 45% or 0. 9% to restore urine output 30-60 ml/hr &038 BP * glucose level approach 250 5% grape sugar added * Incorrect fluid repl > sudden Na &038 cerebral edema * Obtain K level before insulin started insulin > further K * Insulin withheld until fluid resuscitation &038 K>3. 5 * alike rapid IV fluids &038 rapid lowering of glucose cerebral edema Hypersmolar hyperglycemic syndrome HHS * disembodied spirit threatening, able to produce insulin to prevent DKA but not enough to prevent severe hyperglycemia, osmotic diuresis, ECF depletion * Less common than DKA * Often > 60, in DM II Causes > UTI, pneumonia, sepsis, acute illness, new DM II * asymptomatic in early stages > so glucose can rise very high >600mg/dL * The higher glucose > in serum osm > neurologic manifestations somnolence, coma, seizures, hemiparesis, aphasia * Rese mble fortuity (stroke) determine glucose level for correct dx * Ketones absent in urine * Tx similar to DKA * First IV 0. 45% or 0. 9% NS, regular insulin given up after fluid replacement * Glucose fall to 250 add glucose 5% dextrose * Hypokalemia not as significant as in DKA * HHs require greater fluid replacement * Assess VS, I&038O, turgor, labs, cardiac / renal observe related to hydration &038 electrolyte levels, mental status, serum osm Hypoglycemia Low blood glucose glucagon &038 epinephrine > defense against hypoglycemia * s/s of epinephrine > shaking, palpitations, nervousness, diaphoresis, anxiety, hunger, pallor * wag req constant supply of glucose > when > affect mental functioning > LOC, diff speaking, visual disturbances, confusion, coma, death * Hypoglycemis unawareness > no warning signs until glucose reach critical point > incoherent, combative, LOC > lots elderly w/ beta blocker meds * When very high glucose level falls too rapidly, too vigoro us management of hyperglycemia * mismatch in timing of food intake &038 peak of isulin/ OA * Can be quickly reversed Check glucose levels, if contain fat that glucose absorption check glucose in 15 min * Still 70 eat regular meal/snack low peanut butter, bread, cheese, crackers, check glucose in 45 min * No significant imptovement after 2-3 doses of 15g carb MD * Pt not alert to swallow 1mg glucagon IM in deltoid muscle ( nausea, vomiting repercussion hypoglycemia) * Hospital setting > 20-50ml of 50% dextrose IV push * chronic COMPLICATIONS OF DM Angiopathy * end organ dz from damage to blood vessels (angiopathy) 2nd to chronic hyperglycemia * leading cause of diabetes-related deaths, 68% deaths due to cardio, 16% strokes * causes accumul.Of glucose metabolism by products (sorbitol) damage to nerve cells, abnormal glucose molecules in basement tissue layer of small blood vessels (eye,kidney), derangement in RBCs oxygenation to tissues * DM I > keep blood glucose levels near to normal retinopathy &038 nephropathy (complications of microvascular complications) Macrovascular complications * Dz of large, medium size blood vessels , earlier onset in pt w/ diabetes * W > 4-6x risk of cardiovascular dz, M > 2-3 x * risk factors > obesity, smoking, HTN, fat intake &038 sedentary lifestyle * Smoking injurious to pt w/DM, risk for blood vessel dz, CV dz, stroke, lower termination amputations * Maintain BP control bar of CV / renal dz Microvascular complication * Thickening of vessel membranes in capillaries/ arterioles in response to chronic hyperglycemia * Are specific to diabetes Eyes ( retinopathy ), kidneys ( nephropathy ), skin (dermopathy ) * Some changes present w/DM II at time of dx, but s/s not appear until 10-20 yrs after onset of DM * Diabetic retinopathy microvascular damage to retina, most common cause of blindness 20-74 yrs old. Nonproliferative> most common, partial occlusion of small blood vesselin retina microaneurysms, Proloferative& gt most severe, involves retina &038 vitreous neovasculization ( form new blood vessels to compensate) if macula involved vision is lost * DM II > dilated eye exam at time of diagnosis &038 annually, DM I within 5 yrs after DM onset * Laser photocoagulation * Virectomy * Glaucoma Nephropathy microvascular complication, damage to small blood vessels that supply glomeruli / kidney.Leading cause of ESRD in US same risk for DM I &038 II > HTN, smoking, genetic predisposition, chronic hyperglycemia * Screen for nephropathy annually w/ measurement albumin / creatinine ratio * If micro/macroalbuminuria > ACE inh ( lisinopril ) or angiotensin II rec antagonist ( Cozaar ) tx HTN &038 delay progression of nephropathy * Aggressive BP management &038 tight glucose control Neuropathy Sensory neuropathy (PNS) loss of protective sensation in lower extremities amputations * Hyperglycemia > sorbitol &038 fructose take in in nerves damage * Distal symmetric polyneuropathy > hand/ feet bil aterally * Loss of sensation to touch/ temperature * Pain > burning, cramping, crushing, tearing , at night * Paresthesias > tingling , burning, itching * At times skin too small (hyperesthesia) * Foot injury &038 ulcerations without having pain TX blood glucose control, topical creams capsaicin ( Zostrix ) 3-4 X/d pain in 2-3 wks, selective serotonin, norepinephrine reuptake inh ( Cymbalta ), pregabali ( Lyrica ), gabapentin involuntary neuropathy can affect all body systems &038 lead to hypoglycemic unawareness, bowel incontinence, diarrhea, urinary retention Complications * Delayed gastric emptying ( gastroparesis ) anorexia, n/v, reflux, fullness, can trigger hypoglycemia by delaying food absorption * Cardiovascular abnormalities , postural hypotension assess change from lying, sitting, standing, painless MI, resting tachycardia HR * Risk for falls * inner dysfunction > ED in diabetic men > 1st s/s of autonomic failure * Neurogenic bladder > urinary retention, diff. voiding, weak stream empty bladder Q3H in sitting position, Crede maneuver ( work lower abdomen) * Cholinergic agonists > benthanechol Feet &038 lower extremities Risk for theme ulcerations &038 lower extremity amputations * Sensory neuropathy > major rosk for amputations due to loss of protective sensations LOPS * Unaware of foot injury, improper footwear, stepping on objects w/ bare feet * Screening using microfilament > insensitivity to 10g Semmes-Weinstein > risk for ulcers * Proper footwear, avoid injuries, diligent skin care, inspect feet daily * expand risk for amputations due to blood flow to lower extremities * PAD s/s > intermittent claudication, pain at rest, cold feet, loss of hair, cap refill, dependent rubor ( redness when extr in dependent position ) * DX ankle brachial index ABI &038 angiography * Casting to redistribute weight on plantar surface * Wound control > debridement, dressings, vacuum, skin grafting etcetera Charcots foot > ankle &0 38 foot changes joint deformity need fitted footwear * Acanthosis nigricans dark, coarse, thickened skin in flexures &038 neck * Necrobiosis lipoidica diabeticorum DM I, red-yellow lesions w/ atrophic skin , shiny &038 transparent revealing blood vessels under the surface young women * Granuloma annulare DM I, autoimmune, partial rings of papules, dorsal surface of hands/ feet Infection Candida albicans, boils, furuncles, bladder infections (glycosuria) antibiotics Gerentologic * reduction in cells, insulin sensitivity, altered carbohydrate metabolism * 20 % > 65 YO * of conditions treated w/ meds that impair insulin action (