Nutrition final exam

enteral nutrition

anytime nourishment is provided directly to the GI tract (when a patient is not able to eat orally for more than a few days; usually refers to tube feedings”

enteral feeding by tube

appropriate when gut is functioning: Accessible and safe to use when patient is unable or unwilling to consume adequate nutrients/kilocalories orally; physiologic benefits: maintaining gut integrity/function

indications for use of enteral tube feeding

malnutrition risk: 5 days or longer of inadequate or reduced oral intake; severe dysphagia, major burns, short gut, intestinal fistulas, and other situations that produce oral intake

standard intact formulas (polymeric)

require a normally functioning GI tract (blenderized food, milk based, high kilocalories, lactose free, normocaloric, modified nutrients (CHO, fat, protein, vitamins, minerals))

special formulas

hyper caloric, elemental formulas, modular formulas, speciality formulas

hypercaloric (1.5-2. kcal/ml)

designed to meet calorie and protein needs in reduced volume and have a moderate to high osmolality

elemental formulas (predigested or hydroylzed)

composed of partially or fully hydrolyzed nutrients

modular formulas

single macronutrients added to other foods or enteral products

speciality formulas

designed to meet specialized nutrient demands for specific disease states

formulan selection

patients digestive and absorptive capacities, fluid restriction, high metabolic requirements

method of administration - enteral nutrition

continuous, intermittent, bolus

short duration - feeding duration

non-surgical placement

long duration - feeding duration

surgical placement

nasogastric - feeding route

tube is passed through nose to stomach

nasoduodenal - feeding route

tube is passed from nose to duodenum (SI)

nasojejunal - feeding route

tube is passed through nose to jejunum (SI)

esophagostomy - feeding route

tube is surgically inserted into neck and extends to stomach

gastrostomy - feeding route

tube is surgically inserted into stomach

jejunostomy - feeding route

tube is surgically inserted into SI

starting a food

document placement of the feeding tube, position with head of bed elevated 30-45 degrees, increase rate and then concentration

mechanical and GI complications

tube displacement/obstruction, pulmonary aspiration, mucosal damage; diarrhea, nausea, cramping, distention, constipation

metabolic difficulties - tube feeding complications

hyperosmolar dehydration or over-hydration, abnormal blood levels (too high or too low) of: (sodium, potassium, phosphorus, magnesium), hyperglycemia, respiratory insufficiency, rapid weight gain

home enteral nutrition

patients nutritional needs cannot be met orally; enteral access is in place and functioning and patient is tolerating tube feeding regimen; patient or SO is able/willing to perform techniques safely and effectively; disease state is stable, patient is ready for discharge and can be monitored in the home setting; affordable supplies

parenteral nutrition

provision of energy and nutrients intravenously; components of solutions: CHO, amino acids, fats, electrolytes, vitamins, trace elements, total nutrient admixtures (3 in 1 system)

peripheral parenteral nutrition

must be isotonic, limited kilocalories and protein; most often used when short term nutrition support is needed

standard IV - parenteral route

can’t use for hypertonic solutions: less nutrition delivered

PICC line - parenteral route

doesn’t require surgery; inserted in the cephalic, basilic, median basilic, or median cephalic veins and threaded into the superior vena cava; can remain in place for up to 1 year with proper maintenance and without complications

central line - parenteral route

long term, can be with a port, multi lumen

technical, septic, metabolic parenteral nutrition complications

pneumonthorax, subclavian artery puncture, carotid artery puncture, catheter obstruction, thrombosis; catheter related sepsis, septic thrombosis; hyperglycemia, hyperglycemic nonketotic, hyperosmolar dehydration, hypoglycemia, hyperkalemia

sepsis

serious condition resulting from the presence of harmful microorganisms in the blood or other tissues and the body’s response to their presence, potentially leading to the malfunctioning of various organs, shock, and death

home parenteral nutrition

specialized catheter reduces risk of infection; monitoring: laboratory values, temp, weights, glucose measurements, and fluids; HPN at night during sleep (cyclic CPN) to allow freedom to leave home or even work during the day

parenteral to oral or tube feeding

long periods of parenteral nutrition without enteral feedings result in atrophy of the GI tract; minimal enteral intake is encouraged to help maintain normal GI tract physiology and gut mucosal immunity; enteral intake should be documented during weaning

tube to oral feeding

asses patients swallowing ability; stop tube feedings 1 hour before and after meals to promote appetite; as oral intake increases, decrease tube feeding volume; discontinue tube feeding when oral intake consistently exceeds two thirds of estimated energy requirements

cardiovascular disease (CVD)

nearly 50% of all american adults have some form of CVD; 1 in 4 deaths are from heart disease; an american suffers a heart attack every 20 seconds; currently leading cause of death of men and women in the US among all ethnic and racial groups

CVD definition

a group of diseases and conditions that affect the heart and blood vessels including: coronary artery disease (CAD), HTN, peripheral artery disease (PAD), heart failure/congestive heart failure (HF/CHF), congenital heart diseases

metabolic syndrome

a cluster of biochemical and physiological abnormalities associated with the development of CVD and type 2 diabetes

WHR - waist size as risk factor

women: >35 inches; men: >40 inches

atherosclerosis

chronic inflammatory process in which damage to the arterial wall can lead to CAD, stroke, and PAD; begins early in life; vitamin D

angina pectoris - arterial wall damage

lesion in coronary artery causing partially occluded blood flow - resulting in chest pain

myocardial infarction (MI) - arterial wall damage

lesion in coronary artery causing complete occlusion

cerebrovascular accident (CVA) - arterial wall damage

clot (thrombosis) creating a blockage or rupture in cerebral artery impairing blood flow resulting in lack of oxygen to some brain cells

peripheral artery disease (PAD) - arterial wall damage

atherosclerosis in the abdominal aorta, iliac arteries, and femoral arteries produce temporary insufficient blood flow in the arteries on exertion (intermittent claudication) or ischemic necrosis (loss of blood to bone tissue, which causes the bone to die; it is most common in the hips, knees, shoulders, and ankles)

dyslipidemia

LDL to HDL ratio: most often as a result of diet and lifestyle, genetics, may also be triggered by intermittent hypoxemia from sleep apnea

blood cholesterol levels

high density lipoprotein (HDL) cholesterol counteracts the detrimental, pro inflammatory effects of low density lipoprotein (LDL) cholesterol

ATP III classification of serum triglycerides (mg/dL)

<150 Normal; 150-199 Borderline High; 200-499 High; ≥500 Very High

factors that may cause elevated triglycerides

long term excessive alcohol intake, overweight and obesity, physical inactivity, cigarette smoking, very high CHO intake >60% calories, type 2 diabetes, chronic renal failure/nephrotic syndrome, some medications, genetics

systolic pressure

amount of pressure the heart generates when it contracts and pumps out blood

diastolic pressure

the amount of pressure in the arteries when the heart rests between beats

diagnosis high BP

normal (S: less than 120, D: less than 80), elevated (120-129, less than 80), HTN stage 1 (130-139, 80-89), HTN stage 2 (140 or higher, 90 or higher), hypertensive crisis (higher than 180, higher than 120)

forms of HTN

essential (primary, cause not clear): about 95% of HTN cases, prematurity, low birth weight, infections, and poor nutrition - can hamper kidney development, genetics; secondary (cause can be identified): Cushing’s syndrome, primary aldosteronism, renal insufficiency

CVD treatment

lifestyle changes (decreasing alcohol intake, manage weight, increasing physical activity, stop smoking, heart healthy diet), drug therapy (lipid management, antihypertensive medications), physical activity (150 minutes moderate/75 minutes vigorous physical activity/week), nutrition therapy (increase intake of monounsaturated and polyunsaturated fats, reduce intake of saturated fats, increase plant base protein - decrease animal protein, include soluble fiber, include plant sterols and stanols, reduce sodium intake, mediterranean diet, DASH diet)

HTN specific treatment

weight management: most effective, a loss of 10-15 lbs; DASH diet: increase intake of potassium, magnesium, and calcium; decrease intake of sodium: sodium (average intake 3,400mg per day), most added during processing and manufacturing (65%), sodium guidelines (2,300mg per day, if over 40: 1,500mg per day)

mediterranean diet

fresh fruits and vegetables, whole grains, nuts, garlic, fish, and wine in moderation; meat and animal products in small amounts; dairy products: use sparingly, if cheese is used use feta cheese; up to 40% of calories coming from fat, especially extra virgin olive oil

DASH diet

rich in fruits (potassium/magnesium) vegetables (potassium/magnesium), low fat dairy products (calcium); reduced saturated and total fats; reduce sodium intake (sea salt vs table salt; sodium free flavoring options)

nutrient content claims

light or lite: a product has 1/3 fewer kcal than a comparable product or 50% of the fat found in a comparable product, or the sodium content of a low-kcal, low-fat food has been reduced by 50%; reduced or less: a nutritionally altered product that contains 25% less of a nutrient or kcal than the regular product

nutrition therapy after myocardial infarction

start with liquids and progress, as tolerated, to foods of regular consistency; smaller, frequent meals are better tolerated (large meals can increase myocardial oxygen demand by increasing splanchnic (visceral) blood flow; main goal of nutrition therapy is to decrease the workload on the heart)

heart failure or congestive heart failure (CHF), or cardiac decompensation

left ventricle failure produces pulmonary congestion; right ventricular failure results in systemic congestion that causes poor perfusion to all organ systems

nutrition therapy - heart failure

restriction of dietary sodium (mild to moderate heart failure: 3000 mg/day; unresponsive or severe heart failure: 2000 mg/day), fluid restriction if patient is hyponatremic (1 to 2 L/day), mediterranean/DASH diet (rich in antioxidants; rich in unsaturated fats)

acute respiratory failure/distress syndrome (ARDS)

occurs when fluid builds up in the tiny air sacs (alveoli) in your lungs, the fluid keeps your lungs from filling with enough air which means less oxygen reaches your bloodstream, this deprives your organs of the oxygen they need to function; typically occurs in people who are already critically ill or who have significant injuries; severe shortness of breath (main symptom) usually develops within a few hours to a few days after precipitating injury or infection

non acute respiratory distress syndrome

common breathing disorder of premature newborns in which the alveoli in a newborn’s lungs do not remain open because the production of a substance that coats the alveoli (surfactant) is absent or insufficient

nutrition therapy - respiratory failure

most patients require mechanical ventilation, therefore are fed enterally or parenterally; goal is to prevent or treat malnutrition, minimize CO2 production, high calorie, high protein, moderate to high fat, moderate CHO

chronic obstructive pulmonary disease (COPD)

chronic inflammation; air enters easily but becomes trapped; malnutrition occurs: high energy needs for breathing, loss of fat stores and muscle mass, malnutrition (results from altered taste, fatigue, anxiety, depression, increased energy requirements, frequent infections, and side effects of multiple medications)

COPD nutrition therapy

goal: preserve muscle strength and immune system; maximizes oral intake; daily: 25-45kcal/kg, depending on weight status; adequate but not excessive protein to stimulate ventilatory drive (maintenance: 1.2-1.9 g/kg; replenishment: 1.6-2.5 g/kg); non-protein calories: split evenly between CHO and fat; no overfeeding

cystic fibrosis

cause: autosomal recessive disease of mucus-producing exocrine glands: sweat glands, salivary glands, mammary glands, and many glands of the digestive system; characteristics: high sodium and chloride in saliva, tears, and sweat, viscous secretions in pancreas, bronchi, bile ducts, and SI

cystic fibrosis physical signs

growth retardation, failure to gain weight, abdominal protuberance, lack of subcutaneous fat, poor muscle tone, pancreatic insufficiency, pulmonary infections, malabsorption

nutrition therapy - cystic fibrosis

energy needs based on (basal metabolic rate, activity level, lung function, fat absorption), fat (30%-40% of kilocalories), salt (dietary sodium is usually adequate), multivitamins (emphasis on fat soluble, may prescribe water-miscible form if fat malabsorption is severe), enzyme replacement therapy

nutrition therapy - cystic fibrosis for infants and children/adolescents

i: pancreatic enzyme replacements with milk products, breast milk, or formula, supplemental fat or CHO: may be necessary, introduction of solid food as for other infants; C/A: goal: adequate diet and pancreatic enzymes to support growth and maintain nutritional status, monitor closely

asthma

condition in which your airways narrow and swell and produce extra mucus; common triggers are airborne substances, such as pollen, dust mites, mold spores, and pet dander

nutrition therapy - asthma

antioxidant rich diet (oxidative stress plays a role in asthma): fruits, vegetables, whole grains; vitamin C - antioxidant; anti-inflammatory foods: vitamin D, omega 3 fatty acids; healthy gut microbiome: prebiotic foods

tuberculosis (TB)

a potentially serious infectious disease that mainly affects your lungs but can spread to other areas of the body (type 2 diabetes is an individual level risk factor for TB; deficient vitamin D plays a part in etiology); health diet rich in antioxidants and anti-inflammatory nutrients that supports a healthy gut microbiome; medication compliance is often a challenge

metabolic response to stress

metabolism is the process by which your body converts what you eat and drink into energy. during this complex biochemical process, calories in food and beverages are combined with oxygen to release the energy your body needs to function

stress

stress is a normal reaction the body has when changes occur, it can respond to these changes physically, mentally, or emotionally; uncomplicated (altered food intake; altered activity level) vs complicated (trauma; disease); both result in metabolic changes throughout the body

stress response

aldosterone (renal sodium retention), antidiuretic hormone (ADH) (renal water absorption), adrenocorticotropic hormone (ACTH) (adrenal release of cortisol (protein)), catecholamines (renal release epinephrine and norepinephrine (CHO and fat))

metabolic changes: stress vs starvation

major difference: stress - metabolic rate increase vs starvation: metabolic rate decreases

effects of starvation

liver glycogen is used first to maintain normal blood glucose levels and to provide energy for brain and blood cells and is usually depleted within 24 hours; lipid (triglyceride) stores begins and as the amount of liver glycogen decreases free fatty acids are mobilized for energy; after about 24 hours without intake, the prime source of glucose is from gluconeogenesis; during early starvation, the brain uses glucose from the muscle protein (branched-chain amin acids increase in circulation; internal sources of amino acids are lean body mass, vital organs such as the heart muscle, blood proteins, hormones, enzymes; by day 2 or 3 of starvation about 75g of muscle protein is catabolized each day, and other sources of energy such as fatty acids are hydrolyzed from glycerol and released into the bloodstream and can be used by the liver to generate glucose (gluconeogenesis); ketone bodies produced if starvation prolonged

metabolic responses to severe stress

ebb phase: decrease consumption, decrease cardiac output, decrease plasma volume, hypothermia, increase insulin levels, hyperglycemia, hypovolemia, hypotension, increase lactate, increase free fatty acids, increase catecholamines, glucagon, cortisol, insulin resistance; flow phase: increase O2 consumption, increase cardiac output, increase plasma volume, hyperthermia, increase nitrogen excretion, normal or elevated insulin levels, hyperglycemia, normal volume, usual BP, normal lactate, increase free fatty acids, increase catecholamines glucagon and cortisol, increase insulin resistance

deadly cycle

impaired immunity leads to increased risk of disease, disease compromises nutritional status, and compromised nutritional status further impairs immunity

inflammation

homeostasis refers to the ability of the body to maintain a state of internal balance and physical wellbeing in spite of changes or outside factors; to maintain homeostasis the body responds to physiologic or psychologic stress; hormonal and metabolic changes subdue the immune systems ability to protect the body; reactions involve central nervous system and hormones; reactions are determined by magnitude and duration of stress

reducing inflammation

increase intake of anti-inflammatory foods, reduce intake inflammatory foods, manage blood sugar, exercise regularly, manage weight, manage stress, moderate alcohol intake, eliminate the use of tobacco

severe stress - nutrition therapy

protein requirements: normal (0.8 g/kg body weight), moderate stress (1.0-1.5 g/kg body weight), severe stress (1.5-2.0 g/kg body weight); vitamin and mineral requirements also increase; formulas exist to determine the energy needs of patients experiencing hyper metabolic stress; fluids: adults younger than 55 years (35-40 mL/kg body weight), adults 55-65 years (30 mL/kg body weight), adults older than 65 years (25 mL/kg body weight)

effects of stress on protein metabolism

protein metabolism: protein (skeletal muscle) mobilized for energy, decreased uptake of amino acids by muscle tissue, increased urinary excretion of nitrogen, glutamine used as fuel source for intestinal cells - also plays a role in maintaining intestinal immune function and enhancing wound repair

effects of stress on CHO metabolism

hepatic glucose production increased; insulin levels and glucose use increased

effects of stress on fat metabolism

fat from adipose stores is mobilized for energy as the result of elevated levels of catecholamines and concurrent decreased insulin production; fat stores are rapidly depleted if hyper metabolic patients are not fed during this time; resulting malnutrition increases susceptibility to infection

effects of stress on fluid/hydration status

increased fluid losses possible from fever, increased urine output, diarrhea, draining wounds, or diuretic therapy

effects of stress on micronutrient metabolism

need for most vitamins and minerals increases; if kilocalorie needs are met, patients probably recieve adequate amounts of most vitamins and minerals; special attention should be given to vitamins C and A, beta carotene, and zinc; the following supplements are recommended: 500-1000 mg of vitamin C daily, 220 mg of zinc sulfate daily

indirect calorimetry

the standard for determination of resting metabolic rate (RMR) in critically ill patients; RMR based on measurement is more accurate than estimates from predictive equations; overfeeding is