The World Health Organization ( 2014 ) Defines Mental Health

Mental Health SYNOPSIS OF THE TOPIC The World Health Organisation (2014) defines Mental Health â€Å"as a state of well-being in which every individual realises his or her own potential, can cope with the normal stresses of life, can work productively and fruitfully, and is able to make a contribution to her or his community† (para. 1). Mental health refers to an individual’s psychological, emotional and social wellbeing; it has the ability affect people’s perceptions, thought, feelings, actions and capacity to respond to change, stresses and challenges within their lives (Headspace, 2013, para. 1). It influences how individuals perceive themselves, their resilience, life decisions and the people around them. Maintaining a stable, healthy and positive mental state is crucial for all individuals throughout their lives in order to avoid developing mental health problems and illnesses. 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Research Paper Therapeutic Services - 1619 Words

Capstone Research Paper: Therapeutic Services For many Americans, there comes a time when people are in need of therapeutic services and need help finding the right treatment for them and or loved one. Often times therapy is very beneficial to people, but is not always offered with their insurance. Therapeutic services should be provided to all patients as a non-evasive treatment option because these services provide nontraditional alternatives that enhance patient care and therefore, insurance companies should cover these services. Therapeutic services are non-evasive medical therapy. There are many different types of therapy that is out there for people, depending on what treatment they need and what it will be used for. One of the†¦show more content†¦He or she can also evaluate how a person does an activity and make suggestions for doing the activity in a way that is less likely to result in an injury. Another common type of therapy that is frequently needed is psycholog ical therapy that helps people with Psychotherapy, or talk therapy. Psychotherapy is (National Institute of Mental Health). Within this type of therapy, there are different types. Such as cognitive behavioral therapy, CBT for depression, anxiety and bipolar disorders and much more. For example, CBT helps people with depression restructure negative thought patterns. Doing so helps people interpret their environment and interactions with others in a positive and realistic way. It may also help a person recognize things that may be contributing to the depression and help him or her change behaviors that may be making the depression worse (National Institute of Mental Health). Another example of a type of psychotherapy is CBT for bipolar disorder. People with bipolar disorder usually need to take medication, such as a mood stabilizer. But CBT is often used as an added treatment. The medication can help stabilize a person s mood so that he or she is receptive to psychotherapy and can get the most out of it. CBT can help a person cope with bipolar symptoms and learn to recognize when a mood shift is about to occur (National Institute of Mental Health). Although physical and

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

Toro Company

Introduction In the process of organizational management, several strategies are deployed to ensure that organizational goals and targets are met. Some of the strategies deployed include marketing, restructuring and new products launches. The situation presented in this case looks into a company by name of Toro involved in selling snowblowers and lawn products.Advertising We will write a custom case study sample on Toro Company specifically for you for only $16.05 $11/page Learn More The company had been facing problems related to the sale of snowblowers. However, a program launched by the company and an insurance company changed the company fortunes. As an analyst, it is imperative to analyze the changes conducted by the company on different perspectives to see if this program was successful. Program’s Perspective Toro has been conducting good business as a result of the Company’s S’No Risk program. This program made the company sel l more snowblowers through guarantees handed out to distributors. The company took up an insurance policy that cushioned the company from risks related to product recalls. Dick Pollick of Toro was against the continuation of the program given that consumers might not be enthusiastic of the deal in the second year. Toro’s perspective is based on the fact that the snowfall levels might drop slightly meaning customers will be partially funded for their snowblowers (Bell, 1994). As a result, the campaign might put off potential customers in the second year. The insurance in this case offered a good deal to Toro that ensured that the company could not suffer high financial losses as a result of customer product recall. The insurance raised its rates based on past statistics that showed the climate might change leading to decreased snowfall (Albright, 2010). As a result, the insurance had a reason to cushion itself from losses that might result from decreased snowfall in the future leading to massive product recall from customers. Based on the analysis of the sales figures for Toro and the past agreement they had with distributors, it is acceptable for the insurance company to charge 8% of sales as the insurance rate. This is because prior to the No Risk Program, Toro used to offer distributors of its snowblowers a 10% discount for every sale. As a result, if Toro incurred 2% on marketing fees and 8% as insurance rates then it would amount to the 10% rate that was there previously. The risk taken by the insurance company could also cover all regions where snowfall is going to be less than the anticipated levels.Advertising Looking for case study on business economics? Let's see if we can help you! Get your first paper with 15% OFF Learn More Toro customers are pleased with the S’No Risk program which allows them to be repaid for unused snowblowers bought from Toro. However, the paybacks are restructured in a manner that paybacks will be offered when the snowfall falls below 50% of the historical snowfall levels (Bell, 1994). Although, the customer could suffer if snowfall falls below the 70 and 50% levels since no refunds would be availed. The paybacks could be restructured so that customers are repaid through the selling distributor instead of the issue being handled at Toro’s headquarters. Program Analysis The S’No Risk program was successful since sales increased to unprecedented levels and the customers felt that value for money was respected. In the case of Dick Pollick, I think he should continue on the program to protect the sales of the company. The program was successful based on the fact that the company increased its sales at no additional making the company achieve healthy financial margins. In case, management of the S’No Risk program was handed over to me, several factors would have to be looked at. One of the factors that I would look into is the insurance agreement which should be concise to avoid fluctuation in the insurance rates (Albright, 2010). The analysis of the three stakeholders in the case of the S’No Risk program a matrix of common factors they regard highly should be drawn as shown in figure 1. For instance, the customer is susceptible to payback not being respected while Toro is losses resulting from high payback request as a result of poor snowfall. The insurance company would suffer the greatest loss if poor snowfall was to occur in a consecutive manner. The S’No Risk program affects the customer in that the customer might regret purchasing snowblowers from Toro if paybacks take a long time or they are not honored. From Toro’s perspective, the payback form lists that the customer should write his/her name on purchase of the snowblower and mail the form to the company (Grant, 2005). Toro might deny the receipt of the customer forms while the insurance company would want to deal with Toro directly as opposed to the custome rs since the agreement was between them and Toro.Advertising We will write a custom case study sample on Toro Company specifically for you for only $16.05 $11/page Learn More Main Stakeholders Meaning of Scores 9- Very satisfied 4-Somewhat satisfied 1- Dissatisfied Objectives Customer Toro Insurance Be Profitable 1 9 9 Reduce Risks 1 4 9 Guaranteed Payback 9 4 1 Figure 1 Conclusion Insurance companies play a vital role in business because of their risk management line of business. In the case of Toro, the American Home takes care of the risk of product recalls for Toro while the company concentrates on selling its products. The analysis of the S’No Risk program shows that if American Home maintains it insurance rates then Toro could continue to sell its snowblowers without hitches. However, the S’No Risk program has its downside based on poor climatic conditions which could force the insurance companies or Toro to suffer los ses related to paybacks. Customers could also duffer the loss of paybacks taking long to materialize. References Albright, S. Winston, W. (2010). Data Analysis and Decision Making. Chicago, IL: John Wiley and Sons. Bell, D. Schleifer, A. (1994). Decision making under uncertainty. Detroit, MI: Course Technology. Grant, R. (2005). Contemporary strategy analysis. Boston, MA: Greenwood Publishing Group. This case study on Toro Company was written and submitted by user Liberty Z. to help you with your own studies. You are free to use it for research and reference purposes in order to write your own paper; however, you must cite it accordingly. You can donate your paper here.

Learning How to Write an Exploratory Essay by BestEssay.Education

Learning How to Write an Exploratory Essay by Learning How to Write an Exploratory Essay If you are working on an exploratory essay, you are working on a task that is quite unusual. In fact, it is so unusual that as you learn how to write an exploratory essay you will need to momentarily discard much of what you know about writing essays. The reason for this that the approach to writing an exploratory essay is completely different. When writing these essays, your goal is not to prove your thesis or to argue a specific point. Instead, your job is to walk your readers through the things that you have experienced when attempting to solve a problem. What is an Exploratory Essay? It may seem strange to read this, but an exploratory essay is essentially an introspective retrospective. Essentially what you will be doing is examining your approach to defining and solving a problem. The purpose of this essay is to give yourself some good insight on the methods that you use to solve problems, the methods that you use to identify problems, and even your writing style. In many cases, you might write an exploratory essay after completing a research project. What can a Student Get from Writing an Exploratory Essay? In an ideal world, research is objective. People however, are not objective. Each one of us views the world with through the filter of our experiences. This impacts everything we do, including research. An exploratory essay is a way for a student to explore their processes, methodologies, and motivations. When a student completes this process, the goal is that they become a better student and better researcher because they are more aware of themselves. What Questions Should an Exploratory Essay Answer? Here are the questions that you should consider when you write your exploratory essay. Why did I identify this problem as one that I wanted to explore? Why did I select the sources that I did when researching the problem? What made me think that the solution that I applied was the best one? What factors impacted the methods I used to apply the solution? As I read my research notes, what stands out to me about my writing style? Did the solution I applied work? If the solution didn’t work, can I identify any biases or tendencies on my part that contributed to that? Getting Help with your Exploratory Essay Even though this is not a common essay to write, you can still count on to help you with these assignments. We will find the best writer to write an essay of this type or any other type, just for you. Our writers will help you go through your research notes and other information so that your approach and methodology can be identified and explored. When your exploratory essay is finished, you will have an excellent essay to turn in for a grade, and you will also have a great document to refer to when you are questioning the choices that you make when researching a problem or applying solutions.

The Sociology of Gender

The Sociology of Gender The sociology of gender is one of the largest subfields within sociology  and features theory and research that critically interrogates the social construction of gender, how gender interacts with other social forces in society, and how gender relates to social structure overall. Sociologists within this subfield study a wide range of topics with a variety of research methods, including things like identity, social interaction, power and oppression, and the interaction of gender with other things like race, class, culture, religion, and sexuality, among others. The Difference Between Sex and Gender To understand the sociology of gender one must first understand how sociologists define gender and sex. Though male/female and man/woman are often conflated in the English language, they actually refer to two very different things: sex and gender. The former, sex, is understood by sociologists to be a biological categorization based on reproductive organs. Most people fall into the categories of male and female, however, some people are born with sex organs that do not clearly fit either category, and they are known as intersex. Either way, sex is a biological classification based on body parts. Gender, on the other hand, is a  social  classification based on ones identity, presentation of self, behavior, and interaction with others. Sociologists view gender as learned behavior and a culturally produced identity, and as such, it is a social category. The Social Construction of Gender That gender is a social construct becomes especially apparent when one compares how men and women behave across different cultures, and how in some cultures and societies, other genders exist too. In Western industrialized nations like the U.S., people tend to think of masculinity and femininity in dichotomous terms, viewing men and women as distinctly different and opposites. Other cultures, however, challenge this assumption and have less distinct views of masculinity and femininity. For example, historically there was a category of people in the Navajo culture called berdaches, who were anatomically normal men but who were defined as a third gender considered to fall between male and female. Berdaches married other ordinary men (not Berdaches), although neither was considered homosexual, as they would be in today’s Western culture. What this suggests is that we learn gender through the process of socialization. For many people, this process begins before they are even born, with parents selecting gendered names on the basis of the sex of a fetus, and by decorating the incoming babys room and selecting its toys and clothes in color-coded and gendered ways that reflect cultural expectations and stereotypes. Then, from infancy on, we are socialized by family, educators, religious leaders, peer groups, and the wider community, who teach us what is expected from us in terms of appearance and behavior based on whether they code us as a boy or a girl. Media and popular culture play important roles in teaching us gender too. One result of gender socialization is the formation of gender identity, which is one’s definition of oneself as a man or woman. Gender identity shapes how we think about others and ourselves and also influences our behaviors. For example, gender differences exist in the likelihood of drug and alcohol abuse, violent behavior, depression, and aggressive driving. Gender identity also has an especially strong effect on how we dress and present ourselves, and what we want our bodies to look like, as measured by normative standards. Major Sociological Theories of Gender Each major sociological framework has its own views and theories regarding gender and how it relates to other aspects of society. During the mid-twentieth century, functionalist theorists argued that men filled instrumental roles in society while women filled  expressive roles, which worked to the benefit of society. They viewed a gendered division of labor as important and necessary for the smooth functioning of a modern society. Further, this perspective suggests that our socialization into prescribed roles drives gender inequality by encouraging men and women to make different choices about family and work. For example, these theorists see wage inequalities as the result of choices women make, assuming they choose family roles that compete with their work roles, which renders them less valuable employees from the managerial standpoint. However, most sociologists now view this functionalist approach as outdated and sexist, and there is now plenty of scientific evidence to suggest that the wage gap is influenced by deeply ingrained gender biases rather than by choices men and women make about family-work balance. A popular and contemporary approach within the sociology of gender is influenced by symbolic interactionist  theory, which focuses on the micro-level everyday interactions that produce and challenge gender as we know it. Sociologists West and Zimmerman popularized this approach with their 1987 article on doing gender, which illustrated how gender is something that is produced through interaction between people, and as such is an interactional accomplishment. This approach highlights the instability and fluidity of gender and recognizes that since it is produced by people through interaction, it is fundamentally changeable. Within the sociology of gender, those inspired by conflict theory focus on how gender and assumptions and biases about gender differences lead to the empowerment of men, oppression of women, and the structural inequality of women relative to men. These sociologists see gendered power dynamics as built into the social structure, and thus manifested throughout all aspects of a patriarchal society. For example, from this viewpoint, wage inequalities that exist between men and women result from men’s historic power to devalue women’s work and benefit as a group from the services that women’s labor provides. Feminist theorists,  building on aspects of the three areas of theory described above, focus on the structural forces, values, world views, norms, and everyday behaviors that create inequality and injustice on the basis of gender. Importantly, they also focus on how these social forces can be changed to create a just and equal society in which no one is penalized for their gender. Updated by Nicki Lisa Cole, Ph.D.

Without positive freedom, it is impossible to lead a valuable life. Do Essay

Without positive freedom, it is impossible to lead a valuable life. Do you agree - Essay Example Therefore, it is true that valuable life might not be achieved in absence of positive freedom, people need to choose the course of their life and destiny without restrictions, freedom is essential also where individual potential is harnessed for the benefit of the whole society although in the process of enjoying this freedom care should be taken to make sure that other peoples liberty is not violated. In the process of enjoying positive freedom equity in opportunity must be regulated or observed, state may intervene to enforce equity and root out other social evils due to positive freedom (Raz, 1988). In a nutshell, complete absence of positive freedom leads to bad and impossible valuable life because every individual wants to operate in an environment which they feel free not intimidating surroundings, this will increase their productivity that in return improve the living condition and life at large for the whole society. A society that feels able to function without interruption although certain aspects must be observed as mentioned above (MacCallum, 1967). Positive freedom acts as an inner driving force in individuals. This equates and augers well autonomy. At the same time, autonomy many a time equates with several aspects that include individuality, integrity, and freedom of the will, responsibility, and critical reflection. In the same way, factors like self-knowledge, independence, freedom from compulsion, lack of external causation and self assertion play vital roles in perpetuating positive freedom. Different people have got varied notions about the steps that others should take to shape their lives. This is because individuals get involved in activities that portray absence of good morals. It has forced researchers to attempt to identify standing reasons that lie behind dissimilar nature of crimes that individuals commit. Even for all their attempts, the researchers are not able to impose their findings about criminology and its associated