Wednesday, March 13, 2019

Diabetes Mellitus Study Guide

DIABETES MELLITUS * Chronic multisystem dz , abnormal insulin take / stricken use * Disorder of glucose metabolism think to absent/ insuff insulin supply or scurvy utilization of inslin thats avail adequate to(p) * 7th leading realise of closing * leading font of blindness, ESRD, overturn limb amputation * contri merelying factor for effect dz/ stroke bump 2-4 x higher than without DM * INSULIN internal secretion produced by kiosks in islets of Langerhans of pancreas. commonplace continously into melody period ( base rate), or increased w/ repasts (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 intersection by liver, movement of glucose into cells. 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 afterward meal storage of glucose as glycogen in liver/ muscle, inhibits gluconeogenesis, of late deposition, protein synthesis * Nl overnight fasting release of stored gucose from liver, protein from muscle, expound from adipose wind * Skeletal muscle & adipose weave receptors for insulin insulin-dependent tissues p unbalancedow slip I Diabetes Juvenile onco hourg, insulin-dependent, s/s abrupt but dz process subject for several yrs, 5-10%, absent or secondimal insulin production, virus/toxins, chthonic 40, 40% forward 20 yr * s/s thirst( polydipsia), polyuria, polyphagia ( hunger), fatigue, wt loss, Kussmaul rsecond sightirations * immune in nameediate dz T-cells attack & destroy cells * genetic predisposition & exposure to virus * idiopathic diabetes non atoimmune, strongly inherited, in sm all(prenominal) pt w/ fictional character I DM , Afri groundwork/Asian * Predisposition HLAs human leukocyte ntigens when open to viral in fection cells destroyed * Long preclinical period, s/s develop when pancreas ordure no longer produce sufficient insulin to reconcile nl glucose trains * Req. insulin from outside source exogenic insulin eg. injection * No insulin diabetic diabetic acidosis (DKA) life threatening, results in metabolic acidosis * honeymoon period newely diagnosed pts, tx initiated pt encounter remissions req little insulin be crap cells produce suff tot of insulin lasts 3-12 mths then req permanent insulin Prediabetes * run a risk for maturation diabetes glucose trains high but non high enough for diabetes diagnosis * impaired fasting glucose IGF 100-125 mg/dL * 2 hr oral glucose border test OGTT 140-199 mg/dL * HgB A1C 5. 7%-6. 4% risk for diabetes * change magnitude risk for developing DM type II if no noise measures develop DM in 10 yrs * Long term defile to body heart, blood vessels occur in prediabetes * Usually no symptoms * follow healthy weight, exercise evenly, healthy di eting risk of developing diabetes Type II Diabetes * Adult flak, non-insulin dependent, 90% * 35, overweight, tendency to run n families * Afri fecal matter Am, Asian, Hispanics, Amerian Indians Some insulin is produced but either insufficient for body ask / bad utilized * Gradual incursion, many yrs undetected hyperglycemia, 500-1000mg/dL * Early usu. well 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 foe tissue no rejoinder 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 befogged * inappropriate glucose by liver too a lot glucose for body needs type II * substituteed prod. of hormones & cytokines by adipose tissue ( adipokines) place in glucose & fat metabolism type II. Two adipokines ( adiponectin & leptin ) affect insulin esthesia altered mechanism in type I & I * metabolous syndrome risk for type II & cardio dz, cluster of abnormalities, insulin resistance, insulin aims, triglycerides, HDLs, LDLs, HTN * Risk factors for metabolic syndrome of import obesity, sedentary life-style, urbanization, westernization Gestational Diabetes During pregnancy, 7% of pregnancies * High risk flagitious obesity, foregoing hx of gestational DM, glycosuria, polycystic ovary syndrome, family hx of DM II screened at maiden prenatal experience * Average risk OGTT at 24-28 wks of gestation * Higher risk of caesarian section delivery, perinatal death, neonatal complications * Will have nl glucose levels indoors 6 wks postnatal but risk of DM II in 5-10 yrs * Nutritional therapy 1st line , if doesnt work insulin therapy Other specific types of diabetes * Due to other(a) medical condition or treatment causes abn blood glucose levels * Damage , injury, e nd of cell function Cushings, hyperthyroidism, pancreatitis, cystic fibrosis, hemochromatosis, TPN * Meds corticosteroid (prednisone), thiazides, phenytoin(Dilantin), antipsychotics clozapine * Tx be condition, stop meds Diagnostic studies * A1C 6. 5 % greater convenience, no fasting req, little day to day alterations during stress/ illness * FPG 126 no caloric pulmonary tuberculosis for 8 hrs prior exam confirmed by repeated scrutiny 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 entice results.False negative impaired GI absorption, falsely elevated repelling restrictions of carbs, corking illness, meds corticosteroids, contraceptives, chouse 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 settle it regul arly, done 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 well being, check acute complications, prevent/ delay onset/ progression met when pt maintain glucose level as near to nl, daily decisions near solid food usance, blood glucose testing meds, exercise * Rapid acting insulin lispro (Humalog), aspart (NovoLog) onset 0-15 min, roseola 60-90 min, dur. -4 hrs , clear, give 15 min before meals bolus * Short acting fifty-fifty (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 hypoglycaemia, dur. 10-16 hrs, can be mixed w/ unforesightful & rapid, cloudy, must be agitated before adm. Long acting glargine (Lantus), detemir ( Levemir) improver to meal quantify insulin, type I, to manipulate glucose between meals & overnight, without it risk of developing DKA, no peak risk of hypoglycaemia , not diluted or mixed, 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/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 electric refrigerator/ traveling-thermos, Prefilled syringes sight impaired, manual dexterity syringes w/ cudy solution in vertical position needle up to avoid clumping of suspension, rolled gently, tippy before injection. * Injection paunch fastest absorption arm, thigh, buttock, rotate within 1 particular site never into site thats about to be exercised (heat = absorption & onset), vial 1ml=100U, SQ 90 degrees * Needles ? 5/16 go on (short children, thin adults) gauges 28,29,30,31 higher ga uge = itsy-bitsyer diameter = more flourishing injection * Re capital letterping done only by person using syringe, never recap syringe used by pt alcohol swabs in health care facility before inj to HAI, at home muck & water * Insulin pump continuous subq insulin infusion 24 hr/d basal rate , loaded w/ rapid acting insulin via credit card tubing to catheter in subq tissue.At meal time bolus . (+) tight glucose control, similar to nl physical 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 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, nightm ares if in sunup 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 wake in the morning due to release counterregulatory hormones in predawn hrs ( possibly GH/cortisol) adolescence/ late 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 promptly absorbed/eliminated, cause wt gain, take 30 min before meal, not if skipped * Biguanides Metformin glucose lowering, first choice DM II/prediabetes, obese & stiffen blockers slow down carbs absorption, taken with first bite, 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, beat out 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 / curl up diuretic hyperglycemia, K Nutrition Type I meal planning, exercise, genuine w/ pts eating habits & activity pattern in mind, day to day consistency in timing & amount of food eaten * Type II wt loss = improved insulin resistance, total fats & si mple sugars = nutritionists calorie & carbs intake Spacing meals , wt loss 5-7% = glycemic control, regular exercise * Carbohydrates sugar, starches, fiber total grains, fruits, veggies, low fat milk included min 130g/d * Glycemic might 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 nephritic 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 expenditure 2 drinks men, track carbs w/ each meal & daily, set strangulate for max amount ( depends on age, wt, activity level) usu. 45-60g /meal also My benefit & plate method ( ? nonstarchy veggies, ? starch, ? protein, nonfat milk & fruit * work on one hundred fifty min/wk suss out intensity aerobic DM I I 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 * dumbfound 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). in the beginning exercise glucose immediate info about glucose levels can make adjustments diet, activity, meds * Recomm. for all insulin- inured 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 drop dead of meal if effective Pancreas organ transplant * For pt w/ ESRD, plan to have kidney transplant * Pancrea s transplanted following kidney transplant, pancreas solely rare * Pancreas alone only if hx of severe metabolic complications, emotional roblems w/ exogenous insulin, failure of insulin-based focusing * 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 * Pancreatic islet cell transplantation in experimental stage, islets from deceased pancreas via catheter into abdomen portal mineral 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 measure outment bypast hx mumps, rubella, viral inf, recent trauma, stress, pregnancy, infant9lbs, Cushing, acromegaly, family hx of DM * Meds compliance w/ insulin, OA corticostero ids, 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 breathing time * Neuro altered reflexes, restlessness, confusion, coma * 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, DKA, HHS hypersmolar hyperglycemic syndrome * Stress f acute illness/ surgery counterregulatory hormones hyperglycemia ( even minor amphetamine resp infection or flu can cause this) * Continue regular diet, noncaloric changefuls (broth, water, diet gelatin, decaffeinated), take OA/insulin as cocksure, monitor glucose Q4H * Acutely ill DM I , glucose240 test urine for ketones Q3-4H , medium/large history to MD * Ill eat than normal continue OA meds/ insulin as prescribed + kale containing unruffleds (soup, juices, decaffeinated) * Unable to keep fluids/ food down MD * foundert 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 * Intraoperative IV fluids & insulin before, during, after sx when theres no oral intake In DM II w/ OA explain its temporary measure, doesnt 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 check & is nl) * Insulin adm teach proper administration, adjustments, side effects, prise response to insulin tx, if new to insulin assess ability to manage tx safely, cognitive status, ability to recognize/ tx hypoglycemia, if cognitive science a nother 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 doesnt cause hypoglycemia * OA w/ diet & activity, not take extra contraceptive pill when overeating * Diligent peel care & dental aily brushing/ flossing, express dentist about DM * pluck 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 , canalise snacks, extra insulin COMPLICATIONS Diabetic Ketoacidosis DKA * Diabetic coma Profound lack 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 us ed for energy fat broken for fuel ketones (by product) serious when immoderate in blood alter pH, cause metabolic acidosis ketonuria (in urine) & electrolyes humiliated impaired protein synthesis, nitrogen baffled from tissues * Untreated depletion of Na, K, Cl, Mg, phosphate hypovolemiarenal failure/ memory board of ketones & glucose shockcoma (result of dehydration, lytes & acidosis)death * s/s dehydration, poor turgor, dry mm, HR, orthostatic hypotension, Kussmaul , abdominal hassle, drop down eyeballs, acetone fruity odor, early s/s lethargy,weakness * blood glucose 250, arterial blood pH IV access begin fluid/ electrolyte fill-in NaCL 0. 45% or 0. 9% to restore urine output 30-60 ml/hr & BP * glucose 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 Hypersm olar 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) interpret glucose level for correct dx * Ketones absent in urine * Tx similar to DKA * premiere 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, I&O, turgor, labs, cardiac / renal monitoring related to hydration & electrolyte levels, mental status, serum osm Hypoglycemia Low blood glucose glucagon & epinephrine self-abnegation against hypoglycemia * s/s of epinephrine shaking, palpitations, nervousness, diaphoresis, anxiety, hunger, pallor * brain req aeonian supply of glucose when affect mental functioning LOC, diff speaking, visual disturbances, confusion, coma, death * Hypoglycemis unknowing no warning signs until glucose reach critical point incoherent, combative, LOC often venerable w/ beta blocker meds * When very high glucose level waterfall too rapidly, too vigorous management of hyperglycemia * Mismatch in timing of food intake & peak of isulin/ OA * Can be speedily 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 appal to swallow 1mg glucagon IM in deltoid muscle ( nausea, vomiting rebound hypoglycemia) * infirmary setting 20-50ml of 50% dextrose IV push * CHRONIC COMPLICATIONS OF DM Angiopat hy * 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 hyperg lycemia * 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 most severe, involves retina & vitrified 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/macroalbumin uria ACE inh ( lisinopril ) or angiotensin II rec antagonist ( Cozaar ) tx HTN & delay progression of nephropathy * Aggressive BP management & tight glucose control Neuropathy centripetal neuropathy (PNS) loss of preventive sensation in lower extremities amputations * Hyperglycemia sorbitol & fructose accumulate in nerves damage * Distal symmetric polyneuropathy hand/ feet bilaterally * liberation of sensation to touch/ temperature * Pain burning, cramping, crushing, tearing , at night * Paresthesias tickling , 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 emptyin g ( gastroparesis ) anorexia, n/v, reflux, fullness, can initiation hypoglycemia by delaying food absorption * Cardiovascular abnormalities , postural hypotension assess change from lying, sitting, standing, painless MI, resting tachycardia HR * Risk for falls * Sexual disfunction 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, wrongful footgear, 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 of paper risk for amputations due to blood flow to lower ext remities * PAD s/s intermittent claudication, pain at rest, cold feet, loss of hair, cap refill, dependent rubor ( redness when extr in dependent position ) * DX mortise joint brachial index ABI & angiography * Casting to redistribute weight on plantar airfoil * Wound control debridement, dressings, vacuum, skin grafting etc. Charcots 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, 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 fulfil (

No comments:

Post a Comment

Note: Only a member of this blog may post a comment.