Bare Bones Essay examples -- Poetry Analysis

The poem â€Å"Sometimes the Words Are So Close,†(963) written by Julia Alvarez, discusses how words like a person can be stripped down and made uncomplicated. People are full of layers that surround them everyday. Each layer can be discarded one at a time, down to the bare essentials and in that space, people can be who they truly are. This is also where she explores her voice as a woman. Andrea Schaefer said, in reference to the â€Å"33† Sonnet collection, â€Å"...Alvarez further explores the themes of her voice taking flight and the powers of language to effect personal and political change. These poems more explicitly address her Dominican roots and her 'childhood in a dictatorship/ when real talk was punishable by death'...† During another interview, Alvarez stated; â€Å"...The page is where I learned to put together my different worlds, where I've put down the deepest roots...† Although born in New York, Alvarez lived in the Dominican Republic wi th her family for her first ten years. Unfortunately, they had to flee back to the United States as political exiles in 1960. On writing, Alvarez stated, â€Å"...Not understanding the language, I had to pay close attention to each word -- great training for a writer. I also discovered the welcoming world of the imagination and books...† Alvarez's poem addresses the two worlds she grew up in, the Dominican Republic and the United States and the differences of language in each. Through an implied metaphor, the speaker of the poem unveils herself, a line at a time, while simultaneously building upon the â€Å"figure†(7) of the poem to reveal at its core, a woman. â€Å"Words†(1) are often difficult to form into speech, especially when there is a barrier of translating what they mean as opposed to what they say.... ...Sienna M Potts: Siennese.com. Web. 26 Mar. 2012. . Alvarez, Julia. Andrea Schaefer. American Writers: A Collection of Literary Biographies, Supplement 7. Ed. Jay Parini. New York: Charles Scribner's Sons, 2001. From Scribner Writers Series. 26 Mar. 2012. Alvarez, Julia. â€Å"Sometimes the Words Are So Close.† Meyers 963. Kevane, Bridget and Juanita Heredia. 'Julia Alvarez and Juanita Heredia. Latina Self-Portraits: Interviews with Contemporary Women Writers.† Ed. Citizen of the World: An Interview with Julia Alvarez. Albuquerque, N.M.: University of New Mexico Press, 2000. p19-32. Rpt. In Hunter, Jeffrey W. â€Å"Contemporary Literary Criticism.† 274. Detroit: Gale. From Literature Resource Center. 26 Mar. 2012 Meyer, Michael. The Bedford Introduction to Literature. 9th Ed. Boston: Bedford/ St. Martin's, 2012. print.

Diabetes Mellitus Study Guide

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. 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 * Predisposition HLAs human leukocyte ntigens when exposed to viral infection cells destroyed * Long preclinical period, s/s develop when pancreas can no longer produce suffi cient 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 * Usually no symptoms * Maintain healthy weight, exercise regularly, healthy diet risk of developing diabetes Type II Diabetes * Adult onset, non-insulin dependent, 9 0% * > 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 hormones & cytokines by adipose tissue ( adipokines) role in glucose & fat metabolism – type II. Two adipokines ( adiponectin & leptin ) affect insulin sens itivity 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 condition 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 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 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 chang es 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 – hi gher 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, n ight 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 – Ava ndia > 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 e ating habits & activity pattern in mind, day to day consistency in timing & amount of food eaten * Type II > wt loss = improved insulin resistance, total 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 me thod ( ? 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 h rs 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 * Pancreatic 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 trau ma, stress, pregnancy, infant>9lbs, 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 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 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 + 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 * Intraoperative > 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 e ffects, 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 Profound deficiency of insulin > hyperglycemia, ketosis, acidosis, dehydration * Most likely in DM I pts, but someti mes 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 * 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 & K>3. 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, I&O, turgor, l abs, 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 no t 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 d z, 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 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 & 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, norepin ephrine 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 h ands/ 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 (

Deontology: Ethics and Kant Essay

In our world today it is often hard to genuinely decide what in fact is right or wrong. The reason that it is so tough to determine is because of our human nature given everyone has their own opinion. We do not all think the same or think the same actions and consequences have the same effect. It is this reason we analyze situations with ethical theories, such as that of Kant’s deontology. Kant’s theory in its own right has a strong moral foundation in which it seems understandable to decide what is right or wrong. However it has its weakness as well. To me however, I believe Kant’s theory on deontology offers a sound premise for which to determine what is morally right or wrong. Kant’s theory on deontology is a way of assessing one’s actions. One’s actions are either right or wrong in themselves. To determine if actions are right or wrong we do not look at the outcome in deontology. Instead Kant wants us to look at the way one thinks when they are making choices. Kant believes that we have certain moral duties in regards to one’s actions. It is our moral duty that motivates ones to act. Theses actions are driven either by reason or the desire for happiness. Since happiness is differs from person to person, it is conditional. Reason on the other hand is universal and can be applied to all making it unconditional. In Kant’s theory on deontology, actions are either intrinsically right or wrong, which is based largely on reason. Kant says that it is in virtue of being a rational being that we as humans have the capacity to be moral beings. Also that moral law amounts to one’s duty. Kant says duty is grounded in a supreme rational principle, thus it has the form of an imperative. To determine what actions one should take Kant utilized imperatives. Imperatives are a form of instructions that will guide an individual on what one should do. Kant had two classifications between imperatives, hypothetical and categorical. Hypothetical imperatives can apply to one who aspires for a desired outcome. These imperatives allow one to take an action for the method of obtaining a certain outcome, meaning if one has a desired outcome, then they ought to act. Kant has divided hypothetical imperatives into two subcategories, the imperatives of skill and imperatives of prudence. The imperatives of skill are imperatives that lead to an action in which the end result desired would be anything other than happiness. The imperatives of prudence are imperatives that lead one to actions, where the desired outcome is happiness. Kant believes that morality however is not like this. Morality does not tell one how to act in order to achieve a goal. Instead morality is made up of categorical imperatives. Kant taught that morality is universal, meaning it could be applied to all and moral law must be obeyed. He believed that when we act we are using moral law and act on the maxims, or the universal rules, of our actions. Kant’s categorical imperative states one can â€Å"act only on that maxim through which you can at the same time will that it should become universal law. † Kant’s uses categorical imperative commands one to take an action. Before one can act they must analyze the principle on which they are acting. Once they have determined why they are acting, it may no longer be ideal, then it is wrong for one to use that maxim as a basis for taking that action. Kant’s principle of morality is the categorical imperative. This means that as an imperative it is a command and being categorical the command has its whole worth with in itself. The categorical imperative doesn’t have some proposed end as in a hypothetical situation, it has its own rational necessity in its justification. Kant’s principle of morality is essential to â€Å"good will. † This is a will that acts for the sake of duty. It is the only thing that is good without qualification. Thus a good will cannot be made better or worse by the result it produces. Good will is also the basis for a major part of Kant’s theory and that is the Universal Law Formula, which is the basis in which Kant uses to determine whether or not things are morally right or wrong. This formula states that one should act in such a way that your maxim could become a universal law of nature. That is if you took your belief or ideal and applied it to the entire world would it hold true and not contradict itself. Kant’s categorical imperative has two formulations included within it, one being the Formula of Universal Law and the other being the Formula of Humanity. The second formulation, The Formula of Humanity, is a principle under the Formula of Universal Law. Kant’s defines the Formula of Humanity as â€Å"Act in such a way that you always treat humanity, whether in your own person or in the person of any other, never simply as a means, but always at the same time as an end. † This formulation states that one’s actions are immoral if it is using a person as a means to an end. It also has to be understood that Kant’s ideals greatly fall on a matter of agency, whether or not you are in fact the one willing an action that causes a negative outcome even if you did so now the result of that action would do more good. Because you took action you are the agent that caused a negative outcome. The proposed â€Å"better† outcome has no value towards the morality of your action. Kant’s strengths in his theory are that they can be applied to nature as a whole, thus the universal law formula. His theory doesn’t depend on an individual’s virtues or character. His weakness is that his morality is based on one’s personal action and doesn’t take in to account the outlying consequences that could ultimately benefit from that action. With Kant’s theory I believe we can make a more sound argument as an approach to ethics. With Kant we have to take situations and become very specific with them. We focus on what the action is and universalize it. That way no matter where in the world it can apply to everyone and won’t contradict itself. Then and only then we decided if it is morally right. Also Kant’s theory is good because it leave no grey area with its matter of agency. It doesn’t let possibilities of better or worse consequences affect the morality of the action in question. Thus I believe in all Kant has a more promising approach for ethics.

Learn How to Conjugate Monter (to Climb) in French

Learn How to Conjugate Monter (to Climb) in French A very useful verb, the French  monter  means to climb or to go up. You can imagine how many times youll use it, which is why its important to study how to conjugate it so you can say I climbed or he is climbing in French. This lesson will show you how to do just that. Its also important that you do not confuse  monter with  montrer  (to  show). That one  r  can make a big difference in the meaning of your sentence. The Basic Conjugations of  Monter In French, the conjugations of verbs are more complicated than they are in English. While we can use -ing  for the present tense and -ed  for most past tense uses, French requires a different form of the verb for every subject pronoun within each tense. While that does give you five more words to learn for each of the present, future, and imperfect past tenses, they are easier if youve studied similar words. Thats because  monter  is  a  regular -er verb, meaning it uses the same infinitive ending as the majority of French verbs. With each new one you learn, it becomes a little easier to memorize those youre not familiar with. To study the conjugations of  monter, use the chart to match the subject pronoun with the tense of your sentence. This will indicate which ending is added to the verbs stem (or radical),  mont-. For example, I am climbing is  je monte  and we went up is  nous montions. While that seems simple enough, youll definitely want to practice these conjugations in context. Luckily, there are many common  expressions with  monter  for you to use. Present Future Imperfect je monte monterai montais tu montes monteras montais il monte montera montait nous montons monterons montions vous montez monterez montiez ils montent monteront montaient The Present Participle of Monter The  present participle  of  monter  is  montant. Youll notice that this was formed by adding -ant  to the verb stem, another rule that applies to almost every regular -er  verb. Monter  in the Compound Past Tense For the past tense, the  passà © composà ©Ã‚  is an alternative to the imperfect. This is a compound conjugation, so you will need the  auxiliary verb  Ãƒ ªtre  as well as the  past participle  montà ©. The phrase comes together quite easily. Begin by conjugating  Ãƒ ªtre  into the present tense appropriate to the subject, then allow the past participle to indicate that someone has already climbed. For example, I climbed is  je suis montà ©Ã‚  and we climbed is  nous sommes montà ©. More Simple Conjugations of Monter There will be times when you may need to question whether the act of climbing took place or not. For those occasions, you can use the subjunctive. Similarly, if someone will climb only  if  something else happens, the conditional can be used. Though you might not need either the passà © simple  or  imperfect subjunctive, these are good to know. However, theyre used only on occasion, so they do not need to be a priority. Subjunctive Conditional Pass Simple Imperfect Subjunctive je monte monterais montai montasse tu montes monterais montas montasses il monte monterait monta montt nous montions monterions montmes montassions vous montiez monteriez monttes montassiez ils montent monteraient montrent montassent For direct commands and other short sentences, you can skip the subject pronoun and use  the imperative  form  of  monter. Simplify it to  monte  rather than the more formal  tu monte. Imperative (tu) monte (nous) montons (vous) montez

Chemistry Pick Up Lines to Try on Your Crush

Chemistry Pick Up Lines to Try on Your Crush ​The best chemistry pickup line is sure to set off the reaction for chemical attraction! Here is a collection of cute, corny, funny, and possibly even effective chemistry pick up lines. For best effect, wear a lab coat while delivering a chemistry pick-up line. Safety goggles may help you out, but wearing disposable gloves might come across as creepy. If you really want to make an impression, learn a few science magic tricks. Who wouldnt be impressed by your ability to breathe fire or make glowing drinks? Are you made of copper and tellurium? Because youre CuTe.Do you have 11 protons? Cause youre sodium fine.Are you a carbon sample? Because I want to date you.You must be made of uranium and iodine because all I can see is U and I together.Forget hydrogen, youre my number one element.If I was an enzyme, Id be DNA helicase so I could unzip your genes.Chemists do it on the table periodically.Youre like an exothermic reaction. You spread hotness everywhere.Are you made of Fluorine, Iodine, and Neon? Cause you are F-I-Ne.If I had a choice between DNA and RNA, Id choose RNA because it has U in it.Hey baby, Ive got my ion you!According to the Second Law of Thermodynamics, you are supposed to share your hotness with me.You must be a compound of barium and beryllium because youre a total BaBe.Youre hotter than a Bunsen burner turned up all the way.Hey baby, would a little more alcohol catalyze this reaction?I wish I was adenine so I could get paired with U.Your body must be made of oxygen and neon because you are the ONe. You must be chlorine cause you are polarizing my bond.How about we go back to my place and form a covalent bond?If you were an element youd be Francium because youre the most attractive.You are a photon quanta to my valence electron because you excite me to a higher energy level.My favorite attractive force is van der Waals force. Can you feel it? Ill move closer if you cant.You make me hotter than sulfur hydroxide mixed with ethyl acetate.When Im near you I undergo anaerobic respiration because baby, you take my breath away.Im so strongly attracted to you, scientists will have to discover a fifth fundamental force.Lets find our combined volume by displacing the liquid in my waterbed.We have such great chemistry that we should do some biology together.You are the HCl to my NaOH. With our sweet love, we could make an ocean together.Lets get together sometime. You bring your beaker and Ill bring my stirring rod.I want to stick to you like glucose.Are you made of beryllium, gold, and ti tanium? You must be because you are BeAuTi-ful. Are you into science? Because I LAB you!Are you a non-volatile particle? Because you raise my boiling point.Scientists have recently discovered a rare new element called Beautium. It looks like you are made of it.You must be the acid to my litmus paper because every time I meet you I turn bright red.Could you tell me the oxidation state of this atom and your phone number?My name? Its Bond. Covalent Bond.Honey, were a galvanic cell. Cant you feel the electricity flowing between us?You must be a good benzene ring because you are pleasantly aromatic.How about we slip between my beta-pleated sheets and you get to know my alpha-helix?

EFEECTS OF CGI (COMPUTER GENERATED IMAGES) IN THE MEDIA INDUSTRY Essay

EFEECTS OF CGI (COMPUTER GENERATED IMAGES) IN THE MEDIA INDUSTRY - Essay Example Computer generated images in digital media has also acted as a source of information, which has encouraged a participatory culture. This is by ensuring that the political process is more democratic and less elitist (Bennett and Strange, 2011). This paper aims at finding out how computer generated images impact on the media. Political campaigns usually capitalize on new means of communication in order to reach voters. This was evident in the 2008 U.S presidential elections whereby candidates used computer generated images and internet technologies to conduct their campaigns. Many political analysts liken the way President Obama used the internet in 2008 presidential campaigns to President Kennedys first use of television in presidential campaigns in 1960 (Bennett and Strange, 2011). Utilization of new media in political processes has mostly been viewed as a tool of reaching voters, especially the youth who are always reluctant to turn out and vote. Some digital media analysts have maintained that the effect of social sites like Facebook on political behavior of young voters is still largely unknown The proportion of candidates using digital media for electoral processes has been increasing since 1996 when the internet was initially used in the U.S during campaigns, but the use was extremely limited. The first substantial use of the internet for political campaigns occurred in 2000 during the presidential campaigns of Bush and Gore; these campaigns had sophisticated websites (Bennett and Strange, 2011). By 2008, features of digital media were more advanced and widely used in political processes than in previous years. Political analysts observe that the failure to include new media in campaign strategies can adversely affect campaigns. This is because social media has become relevant and cost effective tool for political mobilization and support. For instance, candidates who fail to utilize digital

Weman administration Assignment Example | Topics and Well Written Essays - 750 words

Weman administration - Assignment Example When it comes to intelligence, honesty, and another character traits the current women administrators are valued highly and the public rates them superior to their previous counterparts (Kantor 1). According to Kantor (1), in another survey, majority of American women are now the wage earners and providers in their households. The survey interviewed more than 1400 women; 40% of the women survey were single or divorced while 53% of them were the providers in their households. One-quarter of the married women in the survey said that they were earning more than their husbands. Previously such statistics was nonexistent (Kantor 1). Additionally, Perrett (1) says that colleges are graduating more women administrators than men under the 30 group. Women are currently earning more than men and occupy senior administration positions than men. In most companies, most women are found in senior management positions. Notably, the number of women in senior positions has increased over time. The IBR assessment, which engrosses both registered and privately-owned organizations, portrays that there has been a 4% growth in women in senior management positions from 2011 to 2012, with 24 percent of organizations with women in top management positions globally compared to 20 percent in 2011. Currently, the number of women administrators is at 24% as compared to their male counterparts. Additionally, younger women are earning more than older women; a significant indication that the younger women are getting more powerful. Most companies are employing women in their management and administration due to the proven capability of w omen. Examples of women leaders who appear to be stronger include the German chancellor Angela Merkel, former Google CEO who is now the current Yahoo CEO Marissa Mayer and Mary Bara the CEO of one of the world’s leading car manufacturer, General Motors. In addition, the administration works of the first U.S lady Michelle Obama and the