Diabetes Mellitus Study Guide Free Essays

DIABETES MELLITUS * Chronic multisystem dz , abnormal insulin production / impaired utilization * Disorder of glucose metabolism related to absent/ insuff insulin supply or poor utilization of inslin that’s available * 7th leading cause of death * leading cause of blindness, ESRD, lower limb amputation * contributing factor for heart dz/ stroke risk 2-4 x higher than without DM * INSULIN – hormone produced by cells in islets of Langerhans of pancreas. Normal – continously into bloodstream ( basal rate), or increased w/ meals (bolus) * Normal glucose range 70-120 mg/dL, average insulin secreted daily 40-50 U 0. 6 U/kg * Glucagon, epinephrine, GH, cortisol oppose effects of insulin counterregulatory hormones they blood glucose lebels, stimulate glucose production by liver, movement of glucose into cells. We will write a custom essay sample on Diabetes Mellitus Study Guide or any similar topic only for you Order Now Insulin released from cells – as precursor / proinsulin thru liver enzymes form insulin C-peptide ( C-peptide in serum urine indicator of cell function) * in plasma insulin after meal storage of glucose as glycogen in liver/ muscle, inhibits gluconeogenesis, fat deposition, protein synthesis * Nl overnight fasting release of stored g;ucose from liver, protein from muscle, fat from adipose tissue * Skeletal muscle adipose tissue receptors for insulin insulin-dependent tissues Type I Diabetes Juvenile onset, insulin-dependent, s/s abrupt but dz process present for several yrs, 5-10%, absent or minimal insulin production, virus/toxins, under 40, 40% before 20 yr * s/s thirst( polydipsia), polyuria, polyphagia ( hunger), fatigue, wt loss, Kussmaul respirations * immune mediated dz; T-cells attack destroy cells * genetic predisposition exposure to virus * Idiopathic diabetes – not atoimmune, strongly inherited, in small # pt w/ type I DM , African/Asian * Predispositio n HLAs human leukocyte ntigens when exposed to viral infection cells destroyed * Long preclinical period, s/s develop when pancreas can no longer produce sufficient insulin to maintain nl glucose levels * Req. insulin from outside source exogenous insulin eg. injection * No insulin diabetic ketoacidosis (DKA) life threatening, results in metabolic acidosis * â€Å"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 * risk for developing diabetes glucose levels high but not high enough for diabetes diagnosis * impaired fasting glucose IGF 100-125 mg/dL * 2 hr oral glucose tolerance test OGTT 140-199 mg/dL * HgB A1C – 5. 7%-6. 4% risk for diabetes * Increased risk for developing DM type II – if no preventive measures develop DM in 10 yrs * Long term damage to body heart, blood vessels occur in prediabetes * Usual ly no symptoms * Maintain healthy weight, exercise regularly, healthy diet risk of developing diabetes Type 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 needs / poorly utilized * Gradual onset, many yrs undetected hyperglycemia, 500-1000mg/dL * Early usu. asymptomatic; high risk pt screen annually * Fatigue, recurrent inf, vaginal yeast inf, candida inf, prolonged wound healing, visual changes * Risk factor obesity ( abdominal/ visceral ) * 4 major metabolic abnormalities * insulin resistance tissue no response to insulin / unresp receptors – receptors are located on skeletal muscles, fat liver * ability of pancreas to produce insulin – fatigued from compensatory prod of insulin, ell mass lost * inappropriate glucose by liver – too much glucose for body needs – type II * altered prod. of hormone s cytokines by adipose tissue ( adipokines) role in glucose fat metabolism – type II. Two adipokines ( adiponectin leptin ) affect insulin sensitivity altered mechanism in type I I * Metabolic syndrome risk for type II 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 – severe obesity, prior hx of gestational DM, glycosuria, polycystic ovary syndrome, family hx of DM II screened at 1st prenatal 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 postpartum but risk of DM II in 5-10 yrs * Nutritional therapy – 1st line , if doesn’t work insulin therapy Other specific types of diabetes * Due to other medical co ndition or treatment causes abn blood glucose levels * Damage , injury, destruction of cell function Cushing’s, hyperthyroidism, pancreatitis, cystic fibrosis, hemochromatosis, TPN * Meds corticosteroid (prednisone), thiazides, phenytoin(Dilantin), antipsychotics – clozapine * Tx underlying condition, stop meds Diagnostic studies * A1C 6. 5 % ; greater convenience, no fasting req, less day to day alterations during stress/ illness * FPG 126 – no caloric intake for 8 hrs prior testing ; confirmed by repeated testing another day; if has s/s and FPG126 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 absorption, falsely elevated severe restrictions of carbs, acute illness, meds corticosteroids, contraceptives, bed rest * IFG impaired fasting glucose 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 days ) DM pts should check it regularly, done to monitor success of tx / make changes to tx 6. % – risk of retinopathy, nephropathy, neuropathy dz affecting RBCs – can affect A1C results Treatment * Goals s/s, promote well being, prevent acute complications, prevent/ delay onset/ progression; met when pt maintain glucose level as near to nl, daily decisions about food intake, blood glucose testing meds, exercise * Rapid acting insulin – lispro (Humalog), aspart (NovoLog) – onset 0-15 min, peak 60-90 min, dur. -4 hrs , clear, give 15 min before meals ; bolus * Short acting – Regular (Humulin R, Novolin R) onste ? -1 hr, peak 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 hypoglycemia, dur. 10-16 hrs, can be mixed w/ short rapid, cloudy, must be agitated before adm. Long acting – glargine (Lantus), detemir ( Levemir) addition to mealtime insulin, type I, to control glucose between meals overnight, without it risk of developing DKA, no peak – risk of hypoglycemia , not diluted or mixed, clear; onset 1-2 hrs, dur. 24hrs +, basal * Combination pt don’t want 2 separate injections, 2 type of insulin mixed together, not same control of glucose levels as with basal-bolus; ahort/rapid mixed w/ ntermediate provide both mealtime basal coverage * Storage vials room temperature 4 wks, heat freezing alter insulin, between 32-86 F; avoid direct exp to sunlight, extra insulin in fridge/ traveling-thermos, Prefilled syringes – sight impaired, manual dexterity; syringes w/ c;udy solution in vertical position needle up to avoid clumping of suspension, rolled gently, warm before injection. * Injection abdomen fastest absorption arm, thigh, buttock, rotate within 1 particular site; never into site that’s about to be exercised (heat = absorption onset), vial 1ml=100U, SQ 90 degrees * Needles ? 5/16 inch (short – children, thin adults); gauges 28,29,30,31 – higher gauge = smaller diameter = more comfortable injection * Recapping done only by person using syringe, never recap syringe used by pt; alcohol swabs in health care facility before inj to HAI, at home soap 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 . (+) tight glucose control, similar 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, may 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 – rebound 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 morning 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 â€Å"starch blockers† slow down carbs absorption, taken with â€Å"first bite†, effectiveness check 2 hr postprandial glucose levels * Thiazolidinediones – Avandia â€Å"insulin sensitizers†, for pts w/ insulin resistance, don’t 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 emptying; prefilled pen * Amylin analog Amylin hormone secreted by cells, co secreted w/ insulin Pramlintide (Symlin) is Synthetic , type I II when glucose level not achieved w/ insulin at mealtimes , subq thigh or abdomen NOT arm , not mixed w/ insulin – cause severe hypoglycemia ! * blockers — masks s/s of hypoglycemia, prolong hypoglycemic effects of insulin * Thiazide / loop diuretic — hyperglycemia, K Nutrition Type I meal planning, exercise, developed w/ pt’s eating habits activity pattern in mind, day to day consistency in timing amount of food eaten * Type II wt loss = improved insulin resistance, t otal fats simple sugars = calorie carbs intake; Spacing meals , wt loss 5-7% = glycemic control, regular exercise * Carbohydrates sugar, starches, fiber whole grains, fruits, veggies, low fat milk included min 130g/d * Glycemic index GI describe blood glucose levels 2 hrs after carb meal , GI of 100 = 50g glucose * Fiber intake 14g/1000 kcal * Fats 7% of total calories , 200mg/d cholesterol trans fats * Protein same for diabetes / normal renal function / gen. population, high proein diet not recommended * Alcohol inhibits gluconeogenesis ( breakdown of glycogenglucose) by liver; severe hypoglycemia in pt on insulin / oral hypoglycemic dx. Moderate alcohol consumption 2 drinks men, track carbs w/ each meal daily, set limit for max amount ( depends on age, wt, activity level) usu. 45-60g /meal ; also My Pyramid plate method ( ? nonstarchy veggies, ? starch, ? protein, nonfat milk fruit * Exercise 150 min/wk moderate intensity aerobic; DM II resistance training 3 x wk, most adults should 30 min moderate intensity activity 5 x most 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 snack every 30 min. during exercise (prevent hypoglycemia). Before exercise glucose immediate info 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 after exercise esp in type I, whenever hypoglycemia suspected, when ill (stress), 2 hrs after start 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 management * Improve quality of life, no exogenous insulin need, no dietary restrictions * Only partially able to reverse renal neurologic complications * Need lifelong immunosuppression to prevent rejection * Pa ncreatic islet cell transplantation in experimental 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 chronic complications * Adjust lifestyle to accommodate DM regimen w/ min. stress Nursing assessment Past hx mumps, rubella, viral inf, recent trauma, stress, pregnancy, infant9lbs, Cushing, acromegaly, family hx of DM * Meds compliance w/ insulin, OA; corticosteroids, phenytoin, diuretics * Eyes sunken 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, coma * MS muscle wasting * Also electrolyte abnormalities, fasting gluc ose level 126, tolerance test 200, leukocytosis, BUN, creatinine, triglycerides, cholesterol, LDL, HDL, A1C 45yrs without risk factors for diabetes Acute intervention * Hypoglycemia, DKA, 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 , glucose240 test urine for ketones Q3-4H , medium/large report to MD * Ill eat than normal continue OA meds/ insulin as prescribed + carbohydrate containing fluids (soup, juices, decaffeinated) * Unable to keep fluids/ food down MD * Don’t stop insulin when ill counterregulatory mechanisms will glucose level * Food intake important body needs extra energy to deal w/ stress Extra insulin may be needed to meet this demand, prevent DKA in DM I * Intraoperati ve IV fluids insulin before, during, after sx when there’s no oral intake In DM II w/ OA – explain it’s temporary measure, doesn’t mean worsening of DM * If contrast medium (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 is nl) * Insulin adm teach 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 memory deficit OA or short acting OA cuz doesn’t cause hypoglycemia * OA w/ diet activity, not take extra pill when overeating * Diligent skin care dental aily brushing/ flossing, inform dentist about DM * Foot care !!! scrapes, burns treated promptly monitored nonirritating antiseptic ointment dry sterile pad not start to heal in 24 hrs or infection MD * Regular eye exams * Travel – sedentary walk Q2H to prevent DVT prevent glucose , carry snacks, extra insulin COMPLICATIONS Diabetic Ketoacidosis DKA * Diabetic coma Profo und 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 properly used for energy fat broken for fuel ketones (by product) serious when excessive in blood alter pH, cause metabolic acidosis ketonuria (in urine) electrolyes depleted; impaired protein synthesis, nitrogen lost from tissues * Untreated depletion of Na, K, Cl, Mg, phosphate hypovolemiarenal failure/ retention of ketones glucose shockcoma (result of dehydration, lytes 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 replacement NaCL 0. 45% or 0. 9% to restore urine output 30-60 ml/hr BP * gluco se level approach 250 5% dextrose added * Incorrect fluid repl sudden Na cerebral edema * Obtain K level before insulin started – insulin further K * Insulin withheld until fluid resuscitation K3. 5 * Too rapid IV fluids rapid lowering of glucose cerebral edema Hypersmolar hyperglycemic syndrome HHS * Life 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 * Resemble CVA (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 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, IO, turgor, labs, cardiac / renal monitoring related to hydration electrolyte levels, mental status, serum osm Hypoglycemia Low blood glucose glucagon epinephrine defense against hypoglycemia * s/s of epinephrine shaking, palpitations, nervousness, diaphoresis, anxiety, hunger, pallor * brain 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 often elderly w/ beta blocker meds * When very high glucose level falls too rapidly, too vigorous management of hyperglycemia * Mismatch in timing of food intake 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 rebound 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 membrane of small blood vessels (eye,kidney), derangement in RBCs – oxygenation to tissues * DM I keep blood glucose levels near to normal – retinopathy 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 sedentary lifestyle * Smoking injurious to pt w/DM, risk for blood vessel dz, CV dz, stroke, lower extremity amputations * Maintain BP control – prevention 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 u ntil 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 most severe, involves retina vitreous neovasculization ( form new blood vessels to compensate) if macula involved vision is lost * DM II dilated eye exam at time of diagnosis 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 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 delay progression of nephropathy * Aggressive BP management tight glucose control Neuropathy Sensory neuropathy (PNS)– loss of protective sensation in lower extremities amputations * Hyperglycemia sorbitol fructose accumulate in nerves damage * Distal symmetric polyneuropathy hand/ feet bilaterally * Loss of sensation – to touch/ temperature * Pain burning, cramping, crushing, tearing , at night * Paresthesias tingling , burning, itching * At times skin too sensitive (hyperesthesia) * Foot injury 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 Autonomic neuropathy – can affect all body systems 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 * Sexual 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 ( massage lower abdomen) * Cholinergic agonists benthanechol Feet lower extremities Risk for foot ulcerations 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 * PAD 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 angiography * Casting to redistribute weight on plantar surface * Wound control debridement, dressings, vacuum, skin grafting etc. Charcot’s foot ankle foot changes joint deformity need fitted footwear * Acanthosis nigricans – dark, coarse, thickened skin in flexures neck * Necrobiosis lipoidica diabeticorum – DM I, red-yellow lesions w/ atrophic skin , shiny 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, fur uncles, 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 ( How to cite Diabetes Mellitus Study Guide, Essay examples