Nutrition Therapy for Metabolic Disorder PDF

Nutrition Therapy for Metabolic Disorder Hypoglycemia Blood sugar level concentration of 40 mg/dL and spontaneous hypoglycaemia – distinct to diabetes mellitus. A.​ Fasting hypoglycemia – occurs when hepatic glucose production does not match cellular glucose uptake (72 hours fasting ca...

Nutrition Therapy for Metabolic Disorder Hypoglycemia Blood sugar level concentration of 40 mg/dL and spontaneous hypoglycaemia – distinct to diabetes mellitus. A.​ Fasting hypoglycemia – occurs when hepatic glucose production does not match cellular glucose uptake (72 hours fasting can maintain normal blood glucose level). Fasting hypoglycemia may result from insolinoma and congenital hyperinsulinism B.​ Postprandial hypoglycemia is the outcome of high level insulin secretion after few hours (1.5 – 5 hours) after eating a high carbohydrate meal. Rapid digestion and absorption causes sharp rises of blood sugar level and subsequently over secretion of insulin. S/S =weakness, agitation,, nervousness, mental confusion and sweating. Dietary Management ​ Administration of meal with simple sugar ​ Small frequent and well balance meal to prevent hypoglycaemia ​ Adequate protein and fat Metabolic Syndrome/Insulin resistance syndrome ​ Insulin resistance is accompanied by hypertension, glucose intolerance and dyslipidemia Determinant of metabolic syndrome ​ Postmenopausal women with history of adult obesity ​ Genes ​ Stress-related hormone (HSD 1) ​ High calorie diet ​ Sedentary activity ​ Excess weight with apple shape figure ​ Smoking Dietary management ​ Reducing underlying factors such as obesity and physical activity ​ Achieving and maintaining normal glucose level ​ Lowering lipid risk factor ​ Controlling blood pressure less than 130/85 ​ Prevention of complication such as diabetes and cardiovascular diseases ​ Calories = energy intake according to existing weight, food with lower glycemic index ​ Fats = Limiting food high in saturated fat and trans fatty acid, increase omega 3, omega 6 and vegetables oil ​ Carbohydrate = normal carbohydrate requirement, increase fiber ​ Vitamin and minerals = Vitamin C, B complex and E. Potassium prevent elevation of glucose Adrenocortical insufficiency/Addison’s disease ​ Adrinocortical insufficiency – atrophy of adrenal cortex and consequent loss of hormonal secretion ​ Addison’s disease – is strict insufficiency state ( gland no longer secrete hormone)  ​ Condition that precipitates insufficiency which include TB, cancer, acute infection and excessive body salt loss. Adrenal glands are two small endocrine glands. Each gland consist of two part, the cortex which secretes estrogen, progesterone, androgen and adrenocortical hormone. Medulla elaborate epinephrine and norepinephrine Adrenocortical hormone that maintain nutrient hemeostasis 1.​ Glucocorticoid promote release of amino acid from the muscle and increase glyconeogenesis 2.​ Mineralocorticoid maintains electrolyte balance by increasing potassium urinary excretion, retaining sodium by promoting kidney reabsorption back to plasma. S/S ​ Hypotension, low corticosteroid level, weakness, dehydration, nausea and vomiting, diarrhea, sodium-potassium imbalance. 1/3 of client with adrenal insufficiency have diabetes Treatment ​ Administration of glucocorticoid and mineralocorticoid (prednisone or prednisolone) Nutrition therapy objective: ​ Prevention of hypoglycemia by avoiding fasting ​ Prevention of weight loss through improve appetite and strength ​ Modification of sodium according to drug therapy ​ Prevention of hyponatremia Dietary Management ​ High protein and high carbohydrates ​ Monitor blood glucose, sodium, and potassium ​ B complex and vitamin C to increase metabolic demand. ​ Increase caloric intake if patient is under weight ​ Restrict sugar to prevent over stimulation of insulin ​ Adequate fluid intake Hypothyroidism (Myxedema) ​ Lack of thyroid hormones due to deficient activity and less secretion of the thyroid gland. Myxedema in adult and cretinism develop in fetal life or early infancy result from thyroidism of mother. ​ Occurs primarily in women 30-60 years of age. Approximately 95% are goitrous due defective hormone biosynthesis S/S ​ Apathy, weakness, muscle cramps, weight gain, constipation and menorrhagia ​ Advance hypothyroidism = apathy, bradycardia and sluggish reflexes. ​ Full-blown myxedema = periorbital puffiness, drooping upper eyelid, multiple bruises, dry and flaking skin ​ BMR is decrease by 15 t0 40% Treatment ​ Synthetic hormone or thyroid protein from extract animal thyroid glands Thyroxine, Liothyronine, Liotrix, Levothyroxine Dietary Management ​ Decrease energy utilization (low caloric diet with increase protein) ​ Dietary cholesterol is restricted ​ High fiber and natural laxative (prunes) ​ Goitrogens should be in moderation (cabbage, cassava, peanuts, cauliflower, soybeans) Hyperthyroidism ​ Excessive secretion of thyroid hormones will cause speeding up all bodily processes (8 times more common in females). Severe forms are called Grave’s disease/toxic goiter or thyrotoxicosis. ​ S/S’s are increase appetite but with weight loss, diarrhea, Cardiac and respiratory rate are increase, tremor and nervousness, protrusion of eyeballs (increase pituitary hormones). BMR is increased by 50%. Result in disorder of CHO metabolism, increase protein metabolism, calcium imbalance, creatinine metabolism, decrease serum cholesterol level. Treatment: ​ Therapy is aimed to reduce excessive thyroid hormone production (1. Antithyroid drugs such propylthiouracil and methimazole. 2 Radioactive-iodine therapy or subtotal thyroidectomy) Dietary Management: ​ High calorie, (increase 10-30% in mild cases and 50-60% in advances cases) ​ liberal protein(1-2 g/kg or to correct nitrogen balance) ​ Increase calcium phosphorus, vitamin D, and B complex Gout ​ Disorder in purine metabolism characterized by increase serum uric acid level and deposit of sodium urate(tophi) in soft and bony tissues. Gout may be due to overproduction of uric acid or by inadequate excretion via kidneys. S/Ss ​ Severe joint pains, swelling and redness. Antihyperuricemic drugs are used to lower uric acid level such Colchicine (to control acute articular attack) and allopurinol (maintenance) Dietary management: ​ Purine restricted diet (Internal organs, anchovies, crabfat, sardines, yeast – high purine) ​ Shellfish, dry beans, peas, spinach, mushroom, asparagus, fish, meat – moderate purine) ​ Weight control ​ High fluid intake (3 liter a day) to maintain alkaline pH in urine ​ Sodium is restricted ​ Decrease fat and avoid alcohol consumption ​ Extra protein ​ Avoid patis , toyo and salted foods Chronic obstructive pulmonary disease  ​ Characterized by the persistent obstruction of airflow through the lungs ​ Two main types of COPD o​ Chronic bronchitis - persistent inflammation and excessive secretions of mucus in the airways of the lungs -​ Chronic, productive cough persists for at least 3 months of the year for 2 consecutive years o​ Emphysema - breakdown of the lungs’ elastic structure and destruction of the walls of the bronchioles and alveoli -​ Decrease functional capacity of the lung, barrel chest Causes of COPD ​ Cigarette smoking ​ Infections ​ Exposure to dusts or chemicals ​ Genetic factors - Alpha-1-antitrypsin deficiency ​ Inadequate plasma protein Treatment of COPD ​ Quit smoking ​ Influenza and pneumonia vaccine ​ Bronchodilators ​ Corticosteroids ​ Oxygen therapy ​ Antibiotic after culture and sensitivity test Nutrition therapy ​ Food intake should decline when dyspnea ​ Small, frequent meals and between-meal snacks ​ High-kcalorie, high-protein diet ​ Increase fluid Respiratory Failure ​ Gas exchange between the air and circulating blood is severely impaired ​ Consequences of respiratory failure o​ Hypoxemia - low oxygen levels in the blood o​ Hypoxia - low oxygen content of tissues ​ Hypercapnia - excessive carbon dioxide in the blood (Causing acidosis) Cause: ​ Lung injury ​ Pneumonia or sepsis ​ Physical trauma ​ Neuromuscular disorders ​ Smoke inhalation ​ Airway obstruction Treatment of respiratory failure ​ Oxygen therapy ​ Diuretic – pulmonary congestion ​ Treat infection  ​ Anti-inflammatory Nutrition therapy for respiratory Failure ​ 25 to 35 kilocalories per kilogram body ​ 1.0 to 1.5 grams of protein per kilogram body ​ Fluid restriction for client with fluid in the lung ​ Enteral Feeding: Nutrient-dense formulas (1.5 to 2.0 kcalories per milliliter) for acute lung injuries or ARDS