Download Free Medical Assessment And Management of Patients with Diabetes Mellitus PowerPoint Presentation

Assessment And Management of Patients with Diabetes Mellitus PowerPoint Presentation

DOWNLOAD MEDICAL POWERPOINT PRESENTATION

About This Presentation

Description : Check out this medical PowerPoint presentation titled "Assessment and Management of Patients with Diabetes Mellitus" by Linda Self.

This medical PowerPoint presentation talks about Diabetes Mellitus, a chronic metabolic disorder characterized by hyperglycemia resulting from defects in insulin secretion, insulin action or both. Assessment and management of patients with diabetes mellitus requires a comprehensive approach that includes lifestyle modifications, medication therapy, and regular monitoring.

Tags : Diabetes Mellitus, chronic metabolic disorder, hyperglycemia, defects in insulin secretion, insulin action, Assessment of Diabetes Mellitus, management of Diabetes Mellitus, endocrinology, endocrinology PowerPoint presentation

Published on : Apr 18, 2023 | Views : 981 | Downloads : 0

Shareable Url :

Embed Code :

Comment

Transcript

Slide 1-

Assessment and Management of Patients with Diabetes Mellitus By Linda Self
Slide 2-

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
Slide 3-

Diabetes Type I—beta cells destroyed by autoimmune process Type 2—decreased insulin production and decreased sensitivity to insulin
Slide 4-

Type 1 Diabetes Mellitus Genetic susceptibility Autoimmune Glycosuria Fat breakdown DKA
Slide 5-

Type 2 Diabetes Mellitus Resistance Decreased production Generally no fat breakdown HHNS
Slide 6-

Type 2 Diabetes Mellitus Exercise enhances action of insulin Weight loss is cornerstone of treatment
Slide 7-

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
Slide 8-

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
Slide 9-

Clinical Manifestations Polyuria Polydipsia Polyphagia Fatigue, tingling or numbness in hands, slow healing wounds and recurrent infections
Slide 10-

Diagnostic findings Fasting plasma glucose—125 mg/dL Random sugar >200mg/dL According to text, OGTT and IV glucose tolerance test no longer used routinely—see latest guidelines
Slide 11-

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
Slide 12-

Management Nutritional Exercise Monitoring Pharmacologic Education
Slide 13-

Dietary Management Carbohydrate 45-65% total daily calories Protein-15-20% total daily calories Fats—less than 30% total calories, saturated fats only 10% of total calories Fiber—lowers cholesterol; soluble—legumes, oats, fruits Insoluble—whole grain breads, cereals and some vegetables. Both increase satiety. Slowing absorption time seems to lower glycemic index.
Slide 14-

Dietary Management Consistent, well-balanced small meals several times per day Exchange system or counting carbohydrates
Slide 15-

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
Slide 16-

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)
Slide 17-

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
Slide 18-

Continuous glucose monitoring Subcutaneous sensor in abdomen Download data q72h Evaluates trends and efficacy of treatment over 24h period
Slide 19-

HGB A1C Measures blood levels over 2-3 months (per text) High levels of glucose will attach to hemoglobin Helps to ensure that the patient’s glucometer is accurate
Slide 20-

Ketones Check in pregnancy During illness If BS >240
Slide 21-

Insulin therapy Rapid acting—lispro (Humalog) and insulin aspart (Novolog) onset 15’, peak 60-90’ and last from 2-4 hours Short acting—regular. Onset is 30-60’, peak in 2-3h and last for 4-6 hours. Regular insulin is only kind for IV use.
Slide 22-

Insulin Therapy Intermediate insulins—NPH or Lente. Onset 3-4h, peak 4-12 hours and lst 16-20 hours. Names include Humulin N, Novolin N, Humulin L, Novolin L Long acting—Humulin Ultralente. Onset 6-8h, peak 12-16 h and lasts 20-30h. Peakless insulins: determir and glargine
Slide 23-

Complications of Insulin Therapy Local allergic reactions Systemic allergic reactions Insulin lipodystrophy (lipoatrophy or lipohypertrophy) Insulin resistance Morning hyperglycemia—Dawn phenomenon (nocturnal surges of growth hormone) so give dose at HS not before dinner
Slide 24-

Complications of Insulin Therapy Somogyi effect—nocturnal hypoglycemia followed by rebound hyperglycemia-decrease evening dose of insulin To determine cause, test at HS, 3am and upon awakening
Slide 25-

Methods of Insulin Delivery Pens Jet injectors Insulin pumps—insulin is delivered at .5-2 units/hour. Most common risk of insulin pump therapy is ketoacidosis. Implantable devices Transplantation of pancreatic cells
Slide 26-

Oral antidiabetic agents Sulfonylureas—glipizide, glyburide and glimepiride. Hypoglycemia Biguanides—metformin. Lactic acidosis. Alpha-glucosidase inhibitors—acarbose. Delay absorption of CHO
Slide 27-

Oral Agents Non-sulfonylurea secretagogues—repaglinide. Cause secretion of insulin. Thiazolidinediones—pioglitazone 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.
Slide 28-

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
Slide 29-

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
Slide 30-

Acute Complications of Diabetes Hypoglycemia—50-60 or less DKA HHNS
Slide 31-

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
Slide 32-

Hypoglycemia CNS effects—inability to concentrate, headache, lightheadedness, confusion, memory problems, slurred speech, incoordination, double vision, seizures and even loss of consciousness.
Slide 33-

Hypoglycemic unawareness Related to autonomic neuropathy Will not experience the sympathetic surge—with sweating, shakiness, HA, etc.
Slide 34-

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.
Slide 35-

Diabetic Ketoacidosis Clinical features are: Hyperglycemia Dehydration and electrolyte loss acidosis
Slide 36-

DKA Three main causes: illness, undiagnosed and untreated and decreased insulin Other causes: patient error, intentional skipping of insulin
Slide 37-

Presentation of DKA 3 P’s Orthostatic hypotension Ketosis GI s/s Acetone breath hyperventilation
Slide 38-

Diagnostic Findings of DKA BS between 300-800 Acidosis Electrolyte abnormalities Elevated BUN, creatinine and hct r/t dehydration
Slide 39-

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+
Slide 40-

Nursing Management Administer fluids Insulin Prevent fluid overload Strict I&O Follow lytes ECG monitoring Vital signs Monitor patient responses to treatments
Slide 41-

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
Slide 42-

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
Slide 43-

Medical Management Similar treatment as seen in DKA Watch fluid resuscitation if history of heart failure ECG Lytes monitoring Fluids with potassium replacement
Slide 44-

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
Slide 45-

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
Slide 46-

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
Slide 47-

Diabetic Vascular Diseases Up to 21% of diabetics have retinopathy at time of diagnosis
Slide 48-

Macrovascular Complications Coronary artery disease Cerebrovascular disease Peripheral arterial disease
Slide 49-

Management of Macrovascular Diseases Modify/reduce risk factors Meds for hypertension and hyperlipidemia Smoking cessation Control of blood sugars which will help reduce TG
Slide 50-

Microvascular Complications--Retinopathy Diabetic retinopathy-leading cause of blindness in those 20-74 Blood vessel changes—worst 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
Slide 51-

Microvascular complications-Nephropathy Accounts for 50% of patients with ESRD Earliest clinical sign of nephropathy is microalbuminuria. Warrants frequent periodic monitoring for microalbuminuria—if exceeds 30mg/24h on two consecutive random urines, need 24h urine sample
Slide 52-

Nephropathy Diabetes causes hypertension in renal vessels which cause leaking glomeruli, deposits in narrow vessels, scarring and vascular damage
Slide 53-

Microvascular disease-Nephropathy Medical management: control BP (ACE or ARB) Tx of UTIs Avoid nephrotoxic agents, contrast dyes Low sodium diet Low protein diet Tight glycemic control
Slide 54-

Nephropathy May require dialysis May have co-existent retinopathy Kidney transplantation—success now 75-80% for 5 years Pancreas transplantation may also be performed at time of kidney transplantation
Slide 55-

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
Slide 56-

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.
Slide 57-

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
Slide 58-

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)
Slide 59-

Autonomic Neuropathies Cardiac, gastrointestinal and renal systems Cardiac—myocardial ischemia may be painless GI—delayed gastric emptying with early satiety, nausea, bloating, diarrhea or constipation Urinary retention—decreased sensation of bladder, neurogenic bladder
Slide 60-

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
Slide 61-

Autonomic neuropathy-sudomotor neuropathy Patient will have a decrease or absence of sweating of the extremities with compensatory increase in upper body sweating.
Slide 62-

Autonomic neuropathy—sexual dysfunction Decreased libido in women Anorgasmia ED in men UTI and vaginitis Retrograde ejaculations
Slide 63-

Management of neuropathies Early detection, periodic f/u on patient’s 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
Slide 64-

Foot and Leg Problems Sensory loss Sudomotor neuropathy leads to dry, cracking feet PAD—so poor wound healing/gangrene Lowered resistance to infection
Slide 65-

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
Slide 66-

Special issues Hyperglycemia in the hospital—increased food, decreased insulin, steroids, IV dextrose,overly vigorous treatment of hypoglycemia, inappropriate holding of insulin Hypoglycemia in the hospital—overuse of sliding scale, lack of insulin change when dietary intake withheld, overzealous treatment of hyperglycemia, delayed meals after insulin given Alterations in diet—enteral, TPN and clear liquid diets
Slide 67-

Latest guidelines in diabetes management according to Clinical Advisor
Slide 68-

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
Slide 69-

Risk Factors continued Ethnic groups at high risk—Asian Americans, Native Americans, Latinos, Blacks, Pacific Islanders
Slide 70-

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
Slide 71-

Reducing Risk Weight reduction Exercise of 150 minutes per week Comprehensive diet education
Slide 72-

Controlling blood sugar Hemoglobin A1C less than or equal to 6.5% Fasting plasma glucose <110 Two hour postprandial sugar <140 Comprehensive education
Slide 73-

Treating Type I Diabetes Basal bolus insulin and mealtime rapid-acting insulin analog (lispro, aspart, or glulisine) Basal insulin should include determir or glargine Continuous subcu insulin infusion or pump very effective
Slide 74-

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
Slide 75-

Treating Type I diabetes If poor control—check 2h postprandial and at 2AM Check urine ketones if BS>250
Slide 76-

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 dipeptidyl-peptidase-4 inhibitor (Januvia)
Slide 77-

Using insulin in Type 2 DM Usually will meet patient resistance May benefit from a 70/30 combination Requires frequent blood glucose monitoring
Slide 78-

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
Slide 79-

Cardiac risk factors Treat with statins, Zetia (ezetimibe) or fibrates if TG >400***
Slide 80-

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
Slide 81-

Type 2 diabetes Evaluate treatment response within 3 months HgbA1C >8% in patient who has been educated about DM should begin insulin therapy
Slide 82-

Questions--Discussion