Nutrition-Metabolic- Imbalanced Nutrition

Nutrition-Metabolic- Imbalanced Nutrition Diabetes and Obesity 1. Why are we getting larger? a. Contributors to overweight and obesity Energy Balance Physical Inactivity Environment Genes and Family History v. Medicines i. ii. iii. iv. vi. vii. viii. ix. x. Emotional Factors Smoking cessation Age Pregnancy Lack of sleep b. Medical complications of obesity i. Patients who are obese are not only at risk for a host disease and disorders, but also suffer from low self esteem, impaired body image, depression, diminished quality of life ii. Respiratory: Sleep apnea, greater risk to respiratory infections, Pickwickian syndrome iii. Malignant: endometrial, prostate, colon, breast, gallbladder cancer iv. Psychological: social stigmatization and depression v. Cardiovascular: coronary artery disease, hypertension, left ventricle hypertrophy, cardiomyopathy, accelerated atherosclerosis vi. Central Nervous System: stroke, idiopathic hypertension vii. Obstetric and Perinatal: pregnancy related hypertension viii. Surgical: increased surgical risk and postoperative complication ix. Pelvic: stress incontinence x. Metabolic: type 2 diabetes mellitus, prediabetes xi. Cutaneous: intertrigo, hirsutism xii. Extremity: venous varicosities, lower extremity venous edema 2. Metabolic Syndrome: is a cluster of conditions, that occur together increasing your risk of atherosclerotic heart disease, stroke and diabetes (more than 3) a. Increased blood pressure i. Equal to or greater than 130/85 mm Hg b. High blood glucose level i. Equal to or greater than 100 mg/dL c. Excess body fat around the waist and abnormal cholesterol levels i. Men Equal to or greater than 40 inches (102 cm) Women Equal to or greater than 35 inches (88 cm) ii. Men Asian American 35 inches (90 cm) iii. Women Asian American 32 inches (80cm) iv. BMI > 30 kg/m2 if waist circumference isn’t available d. Elevated triglycerides i. Equal to or greater than 150 mg/dL e. Reduced HDL (“good” cholesterol) i. Men Less than 40 mg/dL Women Less than 50 mg/dL f. Management of Metabolic Syndrome: i. Primary goal: 1. Reduce risk for ASVD - Atherosclerotic Cardiovascular Disease ii. Interventions: 1. Weight loss 5–7% of total weight 2. Increased physical exercise (~30 minutes/day) 3. Healthy eating (decreased intake of sat/trans/cholesterol) 4. Management of other s/s (BP, lipids, BG) iii. ** studies show that added fat and metabolic syndrome is directly correlated to insulin resistant 1. Insulin resistance: can lead to type to diabetes and prediabetes because the beta cells fail to keep up with the body’s increased need for insulin. Without enough insulin glucose builds up in the blood stream DM 3. Diabetes Belt a. Southern portion of the United States i. Population more likely to have type 2 diabetes ii. Obesity and inactivity account for nearly a third of the increased risk for type 2 diabetes iii. African Americans are at a higher risk for type 2 diabetes iv. Less likely to have college degree v. showed that losing 5% to 7% of body weight and getting at least 150 minutes of moderate-intensity exercise each week can reduce the risk of developing type 2 diabetes by nearly 60%. 4. Diabetes: is a chronic disorder of the metabolism that is characterized by a partial or complete deficiency of the hormone insulin. Glucose accumulates in the blood stream and the cells starve for energy. The body breaks down fat to use for energy a. Ethnicity and Diabetes: i. American Indian up to 24.1% + Alaskan Natives 6% ii. Non-Hispanic Whites: 7.6% iii. Non-Hispanic Blacks: 13.2% iv. Asian Americans and Pacific Islanders: 9% 1. Filipinos 11.3% 2. Asian Indians 13.0% 3. Chinese 4.4% v. Hispanics: 12.8% 1. Cuban 9.3% 2. Mexican Americans 13.9% 3. Puerto Ricans 14.8 b. Stats: i. 7th leading cause of death in US ii. Leading cause of blindness iii. Leading cause of kidney failure iv. 60% of non traumatic limb amputations c. The Pancreas- secretes insulin in response to glucose levels in the blood i. Exocrine gland- secretes digest enzymes ii. Endocrine gland 1. Islets of Langerhans 2. 3 cell types a. Beta cells-insulin b. Alpha cellsglucagon c. Delta cellssomatostatin d. Types of Diabetes: i. Gestational = 7% 1. Risk factors: a. Obesity/Dx of PCOS b. Personal history of GDM / Strong family history c. Family history of type 1 or 2 dm d. A1c > 5.7, IGT, IFG ,Glycosuria e. HTN, hyperlipidemia, Hx of CVD f. Ethnicity – Hispanic/Latino, American Indian and Alaska Natives, Asian and African Americans 2. Increased lifelong risk for mother and child for developing type 2 diabetes 3. Screen at 4-12 weeks postpartum for prediabetes 4. 24-28 weeks pregnant women are screened for gestational diabetes ii. T1DM = Type 1 (insulin deficient, beta cells die) 5-10% 1. Risk Factors: a. Not inherited but a generic predisposition combined with immunologic and possibly environmental factors 2. What is Type 1 DM? a. Autoimmune disease resulting in destruction of Beta Pancreatic Cells- absolute deficiency b. Hereditary, environment, autoimmune c. 90% of children with DM have type 1 d. Onset of symptoms occur before age 30 e. Honeymoon phase: just diagnosed, and they get better and healthier will only last weeks to a year  DM will return f. Dawn Phenomenon: it is due to around 3am hormones in your body increase blood glucose (cortisol, growth hormone, epinephrine etc) because your body is preparing to wake up g. Somogi Effect: this is due to the insulin peaking in the middle of the night (hyperglycemia), and due to not having any food to eat the liver secretes glucagon increasing blood glucose h. DKA: diabetic ketoacidosis iii. T2DM = Type 2 (insulin resistant, your body does not have enough insulin for your body)- 90-95% **More prevalent than type 1 DM, can be prevented or delayed in people at high risk for the disease through weight reduction and exercise** 1. Risk Factors: a. family history of diabetes b. sedentary lifestyle c. obesity d. race/ ethnicity (e.g. African American, Latino, Native American, Asian American, Pacific Islander) e. age greater than 45 years f. previously identified impaired fasting glucose (IFG) or impaired glucose tolerance (IGT) g. hypertension ≥140/90 h. HDL ≤35, and/or triglycerides ≥250 i. history of gestational diabetes 2. What is Type 2 DM? a. Body produces insulin, but resistant to its effects or it doesn’t produce enough b. Association with obesity c. More common in persons over age 30 and in the obese category d. 90% to 95% of person with diabetes e. Can be managed with weight loss, exercise, oral medications, and occasionally supplemental insulin may be needed. f. May have it for years and not know it g. The longer A1c is kept <7 during 1st 10 years, the longer the delay of consequences h. Leptin: i. regulated food intake; increased with type 2 DM ii. Makes you not hungry iii. Helps regulate body fat by telling the brain what level of fat is in the body 3. Prevention/Delay of Type 2: a. Refer patients with IGT or IFG or A1c 5.7-6.4 for diabetes selfmanagement education (DSME) and support (DSMS) for diabetics and pre-diabetics b. Targeted wt loss of 5-7% and 150min/wk of moderate exercise c. Third party payer of programs d. Metformin e. Annual monitoring of pre-diabetics f. Annual screening for modifiable risk factors e. Signs and symptoms: i. Three Ps: 1. Polyuria - the need to urinate frequently. 2. Polydipsia - increased thirst & fluid intake. 3. Polyphagia - increased appetite ii. Weight loss iii. Fatigue, weakness, vision changes, lesions slow to heal and recurrent infections, sexual problems iv. Extended illness or sudden v. Dehydration vi. Type 1 = sudden nausea, vomiting and abdominal pain = DKA DIABETE Type I S Type II % of cases 5-10% 90-95% Age of onset < 30 Years > 40 years Characteristics Autoimmune disease, viral infections, genetic Obesity, aging, genetic Primary Problems Destruction of pancreatic beta cells Insulin resistance, Insulin deficiency Insulin Secretion Little or none may be normal, increased or decreased Requires Insulin Always Sometimes f. Diagnostic/Screening Tests for Diabetes i. g. Testing Asymptomatic Adults i. Screen everyone above 45 ii. BMI greater than 25 and at least one other risk factor 1. Hypertensive (> 140/90mmHg or on RX for HTN) 2. Dyslipidemia (HDL<35 or tri > 250) 3. Women with polycystic ovary syndrome 4. A1c > 5.7%, (5.7-6.4% = pre-diabetic) h. Testing for T2DM or Prediabetes in Asymptomatic Children i. Begin at 10 years or puberty 1. Overweight- BMI in 85th percentile 2. Fam history 3. Race/ethnicity 4. Signs of insulin resistance 5. Small for gestational age 6. Maternal hx of DM or GDM during child’s gestation 7. Dyslipidemia- elevated cholesterol or fats in the blood i. Labs: i. Plasma Glucose Levels < 126 ii. A1C < 7%, normal range (4-6%) for first 10 years iii. Fasting lipid level 1. Chol < 200, LDL< 100, HDL> 40, trig < 150 iv. Serum creatinine (<1.2 mg/dL) v. Urinalysis 1. Microalbuminuria, ketones, protein vi. Electrocardiogram 1. Cardiac changes vii. DKA- 1/3 of newly diagnosed present in various degrees of DKA. j. Acute complications of Diabetes i. Hypoglycemia 1. Low blood glucose level (50-60 mg/dL) 2. Causes: too much insulin, oral hypoglycemic agents, too little food, excessive physical activity 3. Signs and Symptoms a. Memory lapses, slurred speech, numbness or lips and tongue, disorientation, seizures, loss of consciousness 4. Management: a. Immediate treatment (15:15) b. Give 15 g of fast acting, concentrated carbohydrate i. 3 or 4 glucose tablets ii. 4 to 6 ounces of juice or regular soda iii. 6 to 10 hard candies iv. 2 to 3 teaspoons of sugar or honey c. Recheck in 15 minutes, retreat if above 70 mg/dL or if symptoms persist more than 10 – 15 minutes and no testing available 5. Glucagon: a. TREATMENT OF HYPOGLYCEMIA b. IM or SQ, buttocks, hips, legs, abdomen c. Repeat in 15 without arousal d. May have c/o nausea 6. IV dextrose: a. Administered ER or hospital when pt. unable to take PO glucose b. Effect seen in minutes c. May have c/o of headache ii. Diabetic Ketoacidosis: 1. Caused by an absence of or inadequate amount of insulin resulting in abnormal metabolism or carbohydrate, protein and fat (low mortality) 2. DKA TYPE ONE: NO INSULIN, BREAKDOWN FATS = KETONES 3. Clinical Features: a. Hyperglycemia >250 mg/dL b. Dehydration c. Acidosis 4. Signs and Symptoms: a. include polyuria, polydipsia, blurred vision, weakness, headache, anorexia, abdominal pain (breakdown of fatty acids), nausea, vomiting, acetone breath, hyperventilation with Kussmaul respirations, and mental status changes b. Patient with DKA: i. low serum bicarbonate and low pH; low PCO2 reflects respiratory compensation (Kussmaul breathing) ii. GI symptoms (anorexia, nausea, vomiting, pain), fruity breath iii. Hypotension or orthostatic hypotension iv. Ketone bodies in blood and urine v. Electrolytes vary according to water loss and level of hydration (<6.5 L and 400-500 mEq of K and Na) vi. Blood glucose levels vary between 300 to 800 mg/ dL c. Treatment of DKA: i. REHYDRATION!!! W/ IV fluid ii. IV continuous infusion of regular insulin 1. Insulin will reverse acidosis 2. Insulin tendency to lower potassium level iii. Reverse acidosis and restore electrolyte imbalance 1. Rehydration  increased plasma volume and decrease K+, insulin enhances the movement of K+ into the cells iv. Monitor: 1. Blood glucose and renal function (before K+ rxn and as treatment progresses) a. Monitor K+ = Arrythmias 2. ECG and electrolyte levels: potassium 3. VS, lung assessments, signs of fluid overload v. Prevention: 1. Blood glucose self-monitoring 2. Management and diagnosis of DM 3. Self-care management skills iii. Sick Day Management 1. When you are sick body reacts by releasing hormones to fight infection, hormones will raise blood sugar levels making it more difficult for insulin to lower blood sugar ** ALWAYS TAKE INSULIN ON SICK DAYS** 2. Rest 3. Give yourself ordered insulin 4. Drink lots of fluids a. If BG > 240 mg/dL = sugarfree fluids b. If BG < 240 mg/dL drink fluids with 10-15 gms of carbos 5. Stick to meal plan a. If can’t eat, try foods with high carbos – small frequent; feedings – popsicles, etc. 45 – 50 gms every 3-4 hours b. If blood sugar level is above 240 drink exra liquids that do not contain sugar 6. Test a. Blood glucose and test for ketones in urine every 3-4 hours b. Ketones 2+ DKA 7. Call Provider if: a. BG > 300 or < 70(or according to your provider’s instructions), ketones mod or 2+,s/s of DKA, diarrhea/vomiting excessive, iv. Hyperglycemic Hyperosmolar Syndrome 1. Caused by a lack of effective insulin (insulin resistance)- high mortality 2. Clinical Features: a. Hyperosmolality >320mOm/dL b. Hyperglycemia > 600mg/Dl 3. HHS TYPE 2: STILL PRODUCING INSULIN, NOT ENOUGH AND BODY WILL NOT BREAKDOWN ITSELF = NO KETONES 4. Osmotic Diuresis- monitor for fluid overload 5. Signs and Symptoms: a. hypotension, profound dehydration, tachycardia, and variable neurologic signs due to cerebral dehydration 6. Patient with HHS: a. Blood Glucose levels 600-1200 mg/dL b. Osmolality exceeds 350mOsm/dL c. Other electrolytes are consistent with severe dehydration d. Hypotension and orthostatic hypotension e. Mental changes 7. Treatment of HHS a. Rehydration!! – 0.9% then 0.45% b. Insulin administration – in smaller doses vs DKA c. Potassium replacement d. Monitor i. Blood glucose and renal function/Urinary output ii. ECG and electrolyte levels: potassium iii. VS, lung assessments, signs of fluid overload e. Prevention i. BGSM ii. Diagnosis and management of diabetes iii. Assess and promote self-care management skills Characteristic Diabetic Ketoacidosis Hyperglycemic Hyperosmolar Nonketotic Syndrome Patient Population Type 1 Diabetes Type II Diabetes Onset Rapid Gradual Blood Glucose > 300mg/dL > 600mg/dL Plasma osmolality < 320 mOsm/L > 320mOsm/L pH of arterial blood < 7.3 > 7.3 Blood ketones Large increase Little or no change Urine ketones Large increase Normal or small increase Urine & breath odor Urine smells like rotten apples; breath smells sweet or like acetone Normal v. Long Term Complications of Diabetes: 1. Macrovascular Complications a. Accelerated atherosclerotic changes b. Coronary artery disease, cerebrovascular disease, and peripheral vascular disease 2. Microvascular Complications a. Diabetic retinopathy and nephropathy i. Kidney Disease: granular surface, decreased function, smaller size, high urine protein b. Addition of Statins may help this 3. Neuropathic changes: a. Peripheral Neuropathy i. Nerve damage, tingling, weakness, burning sensation, numbness b. Autonomic nervous system impairment i. Cardiovascular/GI/Urinary 1. Cardiovascular: tachycardia HR, orthostatic BP, myocardial ischemia and infarction 2. GI: bowel dysfunction, constipation, diarrhea, nocturnal fecal incontinence, Dyspepsia (delayed GI emptying) c. Hypoglycemic unawareness i. Adrenal medulla- pt. no longer aware feels shakiness, sweating, nervousness, and palpitations d. Sudomotor neuropathy i. No sweating except on hands/feet e. Sexual dysfunction 5. Diabetes Management a. Medications i. Oral Anti Hyperglycemic Agents 1. Used alone or in combination with 2. How do they work: Increase insulin production and/ or make tissues more responsive to insulin 3. Time to efficacy: a. Give at least 3 months before adding additional therapy 4. Aspirin, alcohol, sulfonamides, oral contraceptives and MO inhibitors increase hypoglycemic affects 5. Medications a. Second Generation Sulfonylureas and Meglitinides i. batteries for pancreas – gives pancreas more energy to make insulin and increases sensitivity to insulin ii. Help stimulate beta cells to secrete extra insulin iii. Can cause low blood sugar b. Biguanides- Metformin i. like plumbers – fixes a leaking faucet, the liver + increases sensitivity to insulin ii. Stops liver from making glucose and increase sensitivity to insulin iii. Given to prediabetcs iv. Should be stopped w/ radio contrast within 48 hours v. Long term b-12 deficiency c. Thiazolidinediones (TZD) i. locksmiths – gets a sticking lock to work – opens cell doors ii. amplifies insulin sensitivity in body cells (insulin sensitizers) and decrease liver glucose production d. Alpha-glucosidase Inhibitors i. traffic cop – directs CHO to a later exit ii. slow the digestion of starches in your blood iii. Take at start of meal and caused blood glucose to rise more slowly e. SGLT2 Inhibitors – porcelain convenience - causes excess glucose to leave through urine i. Blocks reabsorption of glucose in urine so more is excreted ii. UTI and fungal infections common f. DPP-4 Inhibitors i. blocks the breakdown of insulin ii. Insulin 1. Incretin Mimetics a. Enhances beta cell secretion b. Slows the rate of digestion c. Suppresses glucagon secretion d. Example is Byetta – injectable, Bydureon, Victoza e. Not an insulin – used for type 2 f. Has been linked to pancreatitis (rare), kidney failure, possibly thyroid CA 2. Anti- hyperglycemic Synthetic Analogs a. Synthetic hormone that slows stomach emptying (Symlin) b. Signals short-term satiety c. Used with type 1 and 2 d. Associated with weight loss e. Can increase risk of hypoglycemia f. Monitor patients closely 3. Insulin a. Type 1 - Necessary to sustain life. b. Hormone secreted by Pancreatic Beta Cells c. Allows body to transport glucose into cells d. Lock and Key e. Basal Insulin: Insulin that maintains blood sugar levels steadily during periods of rest and daily activity. i. Example: lantus- lasts up to 24 hours, no peak f. Bolus Insulin: insulin that is secreted during meals and snacks to treat risk in blood sugar i. Example: Humalog, novolog (rapid acting) g. NPH: Humulin N- intermediate acting i. Given 2 times a day ii. Cloudy in appearance iii. Can be mixed with rapid and fast acting iv. Cloudy to clear, clear to cloudy h. Regular Insulin i. Humulin R, Novolin R - Short Acting 1. Onset: 30 - 60 mins 2. Peak: 2 - 4 hrs 3. Duration: 5-7 hrs ii. Give 30 – 60 mins before meals iii. May cause hypoglycemia 4-6 hrs after dose given if no snack eaten iv. Only insulin given IV i. Concentrated insulins i. Given to people who are severe insulin resistant ii. Less # of injection in a day j. Pemixed Insulin i. Ideal for paitents with poor compliance, low cognitive functioning, type 2 diabetes k. Insulin Stoarge i. Refrigerate unopened insulin until expiration date. ii. Opened it can be at room temperature. iii. Discard after 28 days, once opened. iv. Discard all insulin after expiration date. v. Discard if cloudy or clumps. vi. Avoid extreme temperatures. vii. Pen storage varies b. Alternative Therapies: i. Acupuncture ii. Biofeedback/Guided Imagery iii. Yoga iv. Alpha-Lipoic Acid v. Chromium vi. vii. viii. ix. x. Herbal Supplements Magnesium Omega-3s Vitamins Other Supplements c. Self-Blood Glucose Monitoring i. Provides valuable information to guide diabetes management; not intended for day to day monitoring or long term self- care ii. Identifies if treatment is needed immediately iii. Identifies if adjustments needed in medication iv. Empowers patients to manage diabetes and prevent complications v. Can use alternate sites (arms, palms ,thighs and calves) instead of fingers vi. Prevention of DKA vii. A word about monitors viii. Advantages: 1. Near real-time glucose testing q 5 min 2. Shows glucose trends 3. Can be uploaded 4. Alarms for critical levels 5. Less finger sticks 6. Sensor in place for up to 7d 7. Replaces fingersticks for dosing ix. Disadvantages: 1. Readings must be confirmed with finger sticks 2X/day 2. In interstitial fluid so lag time – critical values must be verified 3. Expensive 5-10$/day (sensors) 4. Visual/cognitive/motor deficits limit use 5. Tylenol interferes with CGM readings x. Insulin Pumps 1. Advantages a. More normal lifestyle b. One type of insulin- rapid acting c. Increased precision in insulin dosing d. Allows users to sleep late, or dkip meals e. Some shut down with hypoglycemia 2. Disdvatages a. Expensive b. Increased potential for DKA c. Potential for infection d. Diet: i. Promote and support healthful eating to: 1. Control glycemia, BP,lipids 2. Achieve/maintain body wt goals 3. Delay complications of diabetes ii. Address nutrition needs based on preferences iii. Maintain the pleasure of eating iv. Provide practical tools for meal planning v. MNT – Medical Nutrition Therapy vi. Meal Planning 1. 50-60% carbs a. body’s major source for energy b. legumes, oats, some fruits c. 100% of carbs break down into glucose within 15 minutes- 2hrs after eating d. 15 grams= 1 exchange 2. <300 mg cholesterol 3. fiber 25 g daily 4. Protein a. 10-20% of daily caloric index b. 50% turns into glucose within 3-5 hrs after consumption 5. Fat a. 20-30% daily caloric intake- limit saturated fats b. 10% turns into glucose within 4-5 hours after consumption vii. Glycemic Index: 1. Describes how much a food increases blood glucose; a food with a high glycemic index raises blood glucose more than a good with a medium or low glycemic index 2. Combining starchy food with protein- and fat-containing food slows absorption and glycemic response 3. Raw or whole foods tend to have lower response than cooked, chopped, or pureed foods 4. Eating whole fruits rather than juices decreases the glycemic response due to fiber-slowing absorption viii. Physiologic Insulin Formula 1. Grams Carbohydrates + BG – (target BG) (CHO sensitivity factor) (Glucose Correction Factor) e. Exercise i. The best time for me to exercise is mid to late afternoon 1. A hypoglycemic reaction may occur in response to increased exercise. Clients should avoid exercise during the peak time of insulin. NPH insulin peaks 4-12 hours; therefore, afternoon exercise takes place during the peak of the medication ii. Aids in weight loss and lowers cardiovascular risk iii. Lowers blood glucose by ↑ cell sensitivity to insulin iv. 150 min/wk , strength training > 2X/wk , children 60 minutes /day v. Reduce sedentary time, break up amounts of time spent sitting (q 30 minutes) vi. Check BG a during and p – injest 15gm of CHO a intense exercise. vii. Effects of exercise can last 12-24 hrs. Check frequent BG through the night following a day of intense physical activity. Increased carb consumption needed during times of physical f. Pharmacology for Weight Loss i. Prevention of breakdown of fat in GI tract so ↓ absorption 1. Orlisat (Xenical/Alli) Centrally acting – act on brain pathways that regulate appetite 2. Lorcaserin (Belviq) -Selective Serotonin agonist 3. Liraglutide (Saxenda, Victoza) GLP-1 agonist 4. Naltrexone/Bupropion (Contrave) - opioid antagonist/antidepressant g. Metabolic/ Bariatric Surgery i. Metabolic surgery may be considered for adults with BMI >40kg/m and type 2 DM, especially if diabetes or associated comorbidities are difficult to control with lifestyle and pharmacological therapy ii. Risks for patient 1. 2. 3. 4. 5. 6. 7. 8. Wound dehiscence Stomal strictures Erosions or ulcers Postprocedure diarrhea Malabsorption Nutritional and vitamin deficiency Dumping Syndrome Anastomotic leaks with a potential for mediastinitis or peritonitis. iii. Diet after surgery 1. Clear liquid for 2-3 days p surgery 2. Pureed/Protein foods X 2w 3. Small frequent (6) meals 4. Chew – 20-30 min/meal 5. No fluids with meals/small sips – up to 8c/day 6. Avoid concentrated sweets 7. High protein 8. Multi w/fe 9. B 12, Calcium (1200 +D) 10.