Assessment and Management of Patients with Diabetes Mellitus

Assessment and Management of Patients with Diabetes Mellitus

Assessment and Management of Patients with Diabetes Mellitus By Linda Self Growing problem Estimated 7% of US population is diabetic Twice that many have prediabetes 21% of those over 60 have diabetes

45% of new diagnoses are being made in children and adolescents Diabetes Type Ibeta cells destroyed by autoimmune process Type 2decreased insulin production and decreased sensitivity to insulin Type 1 Diabetes Mellitus

Genetic susceptibility Autoimmune Glycosuria Fat breakdown

DKA Type 2 Diabetes Mellitus Resistance Decreased production

Generally no fat breakdown HHNS Type 2 Diabetes Mellitus Exercise enhances action of insulin Weight loss is cornerstone of treatment Gestational Diabetes Glucose intolerance during pregnancy Placental hormones contributes to insulin

resistance High risk: glycosuria, family history, marked obesity Native Americans, African Americans, Hispanics and Pacific Islanders Gestational Diabetes Women of average risk tested between 24-28 weeks of gestation Goals for glucose levels during

pregnancy are 105 or less before meals; 130 or less after meals Will have greater risk of developing Type 2 DM later in life if weight not controlled Clinical Manifestations

Polyuria Polydipsia Polyphagia Fatigue, tingling or numbness in hands, slow healing wounds and recurrent infections Diagnostic findings

Fasting plasma glucose125 mg/dL Random sugar >200mg/dL According to text, OGTT and IV glucose tolerance test no longer used routinely see latest guidelines Gerontologic

Considerations Elevated blood glucose levels are also age related Increase with advancing age Causes may be: increased fat tissue, decreased insulin production, physical inactivity, decrease in lean body mass Management

Nutritional Exercise Monitoring Pharmacologic Education

Dietary Management Carbohydrate 45-65% total daily calories Protein-15-20% total daily calories Fatsless than 30% total calories, saturated fats only 10% of total calories Fiberlowers cholesterol; solublelegumes, oats, fruits Insolublewhole grain breads, cereals and some vegetables. Both increase satiety. Slowing absorption time seems to

lower glycemic index. Dietary Management Consistent, well-balanced small meals several times per day Exchange system or counting carbohydrates

Exercise and Diabetes Exercise increases uptake of glucose by muscles and improves utilization, alters lipid levels, increases HDL and decreases TG and TC If on insulin, eat 15g snack before beginning Check BS before, during and after exercising if the exercise is prolonged

Exercise and Diabetes Avoid trauma to the feet Avoid pounding activities that could cause vitreous hemorrhage Caution if CAD Baseline stress test may be indicated (especially in those older than 30 and with 2 or more risk factors for CAD)

Glucose monitoring Patients on insulin should check sugars 2-4 times per day Not on insulin, two or three times per week (according to text) Should check before meals and 2 hours after meals Parameters from physician very important

Continuous glucose monitoring Subcutaneous sensor in abdomen Download data q72h Evaluates trends and efficacy of treatment over 24h period

HGB A1C Measures blood levels over 2-3 months (per text) High levels of glucose will attach to hemoglobin Helps to ensure that the patients glucometer is accurate Ketones

Check in pregnancy During illness If BS >240 Insulin therapy Rapid actinglispro (Humalog) and

insulin aspart (Novolog) onset 15, peak 60-90 and last from 2-4 hours Short actingregular. Onset is 30-60, peak in 2-3h and last for 4-6 hours. Regular insulin is only kind for IV use. Insulin Therapy Intermediate insulinsNPH or Lente. Onset 3-4h, peak 4-12 hours and lst 1620 hours. Names include Humulin N, Novolin N, Humulin L, Novolin L

Long actingHumulin Ultralente. Onset 6-8h, peak 12-16 h and lasts 20-30h. Peakless insulins: determir and glargine Complications of Insulin Therapy Local allergic reactions Systemic allergic reactions Insulin lipodystrophy (lipoatrophy or lipohypertrophy)

Insulin resistance Morning hyperglycemiaDawn phenomenon (nocturnal surges of growth hormone) so give dose at HS not before dinner Complications of Insulin Therapy Somogyi effectnocturnal hypoglycemia followed by rebound hyperglycemiadecrease evening dose of insulin To determine cause, test at HS, 3am and

upon awakening Methods of Insulin Delivery Pens Jet injectors Insulin pumpsinsulin is delivered at .52 units/hour. Most common risk of insulin pump therapy is ketoacidosis. Implantable devices Transplantation of pancreatic cells

Oral antidiabetic agents Sulfonylureasglipizide, glyburide and glimepiride. Hypoglycemia Biguanidesmetformin. Lactic acidosis. Alpha-glucosidase inhibitorsacarbose. Delay absorption of CHO

Oral Agents Non-sulfonylurea secretagoguesrepaglinide. Cause secretion of insulin. Thiazolidinedionespioglitazone and rosiglitazone. Sensitize. Weight gain.Fertility. Liver. Pramlintide (Symlin). Analogue of amylin. Used with insulin. Injection. Exanatide (Byetta). Incretin mimetic. Causes

satiety. Wt loss. Januvia. Teaching Plan Education is critical Simple pathophysiology Treatment modalities Recognition, treatment and prevention of acute complications When to call the doctor

Foot care, eye care, general hygiene, risk factor management Teaching patients to administer insulin Storing insulin (may not refrigerate if used

within one month). Prefilled syringes should be stored standing up. Syringes Concentrations of insulin Mixing insulins Do not rotate area to area, use same anatomic area No need to aspirate Acute Complications of

Diabetes Hypoglycemia50-60 or less DKA HHNS Hypoglycemia Caused by too much insulin or oral agents, too little food or excessive physical activity Surge in epinephrine and norepinephrine

results in sweating, tremors, tachycardia, palpitations, nervousness and hunger Hypoglycemia CNS effectsinability to concentrate, headache, lightheadedness, confusion, memory problems, slurred speech, incoordination, double vision, seizures and even loss of consciousness.

Hypoglycemic unawareness Related to autonomic neuropathy Will not experience the sympathetic surgewith sweating, shakiness, HA, etc. Treatment for hypoglycemia 2-3 tsp. of sugar or honey

6-10 hard candies 4-6oz. of fruit juice or soda 3-4 commercially prepared glucose tablets Recheck BS 15 minutes, same s/s, repeat treatment. After improvement, then cheese and crackers or milk. Extreme situations, give glucagon. (can cause n/v). D50W.

Diabetic Ketoacidosis 1. 2. 3.

Clinical features are: Hyperglycemia Dehydration and electrolyte loss acidosis DKA Three main causes: illness, undiagnosed and untreated and decreased insulin Other causes: patient error, intentional skipping of insulin

Presentation of DKA 3 Ps

Orthostatic hypotension Ketosis GI s/s Acetone breath hyperventilation Diagnostic Findings of DKA

BS between 300-800 Acidosis Electrolyte abnormalities Elevated BUN, creatinine and hct r/t dehydration Medical Management of

DKA Rehydrate with normal saline, then follow with .45% NaCl then D5.45NS (or other) Restore electrolytes ECGs Hourly blood sugars IV insulin Avoid bicarbonate as can affect serum K+

Nursing Management

Administer fluids Insulin Prevent fluid overload Strict I&O Follow lytes ECG monitoring Vital signs Monitor patient responses to treatments Hyperglycemic

Hyperosmolar Nonketotic Syndrome Predominated by hyperosmolarity and hyperglycemia Minimal ketosis Osmotic diuresis Glycosuria and increased osmolarity Occurs over time Blood sugar is usually over 600

HHNS Occurs more often in older people Type 2 diabetes mellitus No ketosis

Do not usually have the concomitant n/v Hyperglycemia, dehydration and hyperosmolarity may be more severe than in DKA Medical Management Similar treatment as seen in DKA Watch fluid resuscitation if history of heart failure ECG

Lytes monitoring Fluids with potassium replacement Nursing Management of HHNS

Monitor neurologically Monitor ECG Monitor vital signs Labs Hourly blood glucose monitoring Insulin IV Cautious correction of hyperglycemia to

avoid cerebral edema Long term complications of Diabetes Increasing numbers of deaths from cardiovascular and renal complications Renal (microvascular) disease is more common in type 1 diabetics Cardiovascular disease (macrovascular) complications are more common in type

2 diabetics Diabetic Vascular Diseases Chronic hyperglycemia causes irreversible structural changes in the basement membranes of vessels. Result is thickening and organ damage. Glucose toxicity affects cellular integrity Chronic ischemia in microcirculatory

brances>>cause connective tissue hypoxia and microischemia Diabetic Vascular Diseases Up to 21% of diabetics have retinopathy at time of diagnosis Macrovascular Complications

Coronary artery disease Cerebrovascular disease Peripheral arterial disease Management of Macrovascular Diseases

Modify/reduce risk factors Meds for hypertension and hyperlipidemia Smoking cessation Control of blood sugars which will help reduce TG Microvascular Complications--Retinopathy Diabetic retinopathy-leading cause of blindness

in those 20-74 Blood vessel changesworst case scenario, proliferative retinopathy. Also an increased incidence of cataracts and glaucoma in diabetics. Need regular eye exams Control BP, control BS and cessation of smoking can help Microvascular

complications-Nephropathy Accounts for 50% of patients with ESRD Earliest clinical sign of nephropathy is microalbuminuria. Warrants frequent periodic monitoring for microalbuminuriaif exceeds 30mg/24h on two consecutive random urines, need 24h urine sample Nephropathy

Diabetes causes hypertension in renal vessels which cause leaking glomeruli, deposits in narrow vessels, scarring and vascular damage Microvascular diseaseNephropathy Medical management: control BP (ACE or ARB) Tx of UTIs Avoid nephrotoxic agents, contrast dyes

Low sodium diet Low protein diet Tight glycemic control Nephropathy May require dialysis May have co-existent retinopathy Kidney transplantationsuccess now 7580% for 5 years Pancreas transplantation may also be performed at time of kidney

transplantation Neuropathies Group of diseases that affect all types of nerves. Includes peripheral, autonomic and spinal nerves.

Prevalence increases with duration of the disease and degree of glycemic control Neuropathies Capillary basement membrane thickening and capillary closure may be present. May be demyelination of the nerves, nerve conduction is disrupted. Two most common types of neuropathy are: sensorimotor polyneuropathy and

autonomic neuropathy. Peripheral neuropathy Manifestations:paresthesias, burning sensations, numbness, decrease in proprioception. Charcot foot can result from abnormal weight distribution on joints secondary to lack of proprioception

Management of Peripheral Neuropathies Pain management in the form of TCAs, Dilantin, Tegretol, Neurontin, mexilitene, and TENS. Cymbalta has been recommended. Also, the drug Lyrica (pregabalin) Autonomic Neuropathies Cardiac, gastrointestinal and renal systems

Cardiacmyocardial ischemia may be painless GIdelayed gastric emptying with early satiety, nausea, bloating, diarrhea or constipation Urinary retentiondecreased sensation of bladder, neurogenic bladder Autonomic neuropathy hypoglycemia unawareness No longer feel shakiness, sweating,

nervousness and palpitations associated with hypoglycemia The inability to detect warning signs of hypoglycemia can place the patient at very high risk Autonomic neuropathysudomotor neuropathy Patient will have a decrease or absence of sweating of the extremities with compensatory increase in upper body

sweating. Autonomic neuropathy sexual dysfunction

Decreased libido in women Anorgasmia ED in men UTI and vaginitis Retrograde ejaculations Management of neuropathies Early detection, periodic f/u on patients with cardiac disease

Monitor BP frequently for s/s orthostatic hypotension Low fat diet, frequent small meals, close BS monitoring and use of prokinetic medications Meticulous skin care Foot and Leg Problems Sensory loss Sudomotor neuropathy leads to dry,

cracking feet PADso poor wound healing/gangrene Lowered resistance to infection Management of Foot and Leg Problems Teaching patient foot care-inspect feet and shoes daily Examine feet every time goes to doctor See podiatrist at least annually

Closed toe shoes Trimming toenails Good foot hygiene Glycemic control is the key to preventing complications Special issues Hyperglycemia in the hospitalincreased food, decreased insulin, steroids, IV dextrose,overly vigorous treatment of hypoglycemia,

inappropriate holding of insulin Hypoglycemia in the hospitaloveruse of sliding scale, lack of insulin change when dietary intake withheld, overzealous treatment of hyperglycemia, delayed meals after insulin given Alterations in dietenteral, TPN and clear liquid diets Latest guidelines in diabetes

management according to Clinical Advisor Risk factors for Diabetes Mellitus Family history Cardiovascular disease Obesity Sedentary lifestyle History of impaired fasting glucose or impaired

glucose tolerance Hypertension PCOS Gestational diabetes

Risk Factors continued Ethnic groups at high riskAsian Americans, Native Americans, Latinos, Blacks, Pacific Islanders Recommended Screening Fasting glucose levels Oral glucose tolerance testing using 75g of Glucola Fasting glucose of

100-125mg/dL=prediabetes Fasting level >126 is diagnostic OGTT>200 is diagnostic Reducing Risk

Weight reduction Exercise of 150 minutes per week Comprehensive diet education Controlling blood sugar Hemoglobin A1C less than or equal to 6.5% Fasting plasma glucose <110 Two hour postprandial sugar <140

Comprehensive education Treating Type I Diabetes Basal bolus insulin and mealtime rapidacting insulin analog (lispro, aspart, or glulisine) Basal insulin should include determir or glargine Continuous subcu insulin infusion or pump very effective

Treating Type I diabetes Pump is ideal for those with very brittle diabetes or hypoglycemic unawareness Pump also very useful in pregnant women Symlin (pramlintide) should be considered to enhance glycemic control and control weight Treating Type I diabetes

If poor controlcheck 2h postprandial and at 2AM Check urine ketones if BS>250 Type 2 diabetes Diagnosed 9-12 years after they develop the condition HgbA1C 6-7% needs monotherapy Choices are: thiazolidinedione, metformin, insulin secretagogue

(sulfonylureas, Prandin), alpha glucosidase inhibitor or a dipeptidylpeptidase-4 inhibitor (Januvia) Using insulin in Type 2 DM Usually will meet patient resistance

May benefit from a 70/30 combination Requires frequent blood glucose monitoring Cardiac risk factors 50% of those with Type 2 Diabetes Mellitus have hypertension, 25% in type 1 Need ARB or ACE inhibitor Dyslipidemia needs to be addressed goal of LDL <100 (<70 if DM and CAD);

HDL >40 in men and >50 in women, TG <150 Cardiac risk factors Treat with statins, Zetia (ezetimibe) or fibrates if TG >400*** Nutrition CHO 45-65% of total calories Protein 15-20%

Fiber intake 25-50g/day---blunts the glycemic response Dietary fat <30% w/saturated fat <10% and cholesterol <300mg/day Type 2 diabetes Evaluate treatment response within 3

months HgbA1C >8% in patient who has been educated about DM should begin insulin therapy Questions--Discussion

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