Nutrient Metabolism; 35 questions Concepts of nutrition; 19 (w/ 4 that r diet specific) Malnutrition; 3 questions Diabetes; 10 Obesity; 3

Concepts of nutrition; 19 (w/ 4 that r diet specific)

• Provides: – Energy for cellular metabolism and repair– Organ function– Growth– Body movement

• Basal metabolic rate (BMR): Energy needs while at rest• Affected by:

• Age/gender • Body mass Starvation Lactation• Menstruation Pregnancy• Fever/illness/infections/injury• Activity level Thyroid function

• Resting energy expenditure: BMR +– Energy needed for all BMR activities and energy to digest food and do some mild activity– REE = 60% to 75% of daily needs

Nutrients Nutritional value : Nutrient density (Proportion of nutrients to # of Kcal) Low and high

• Carbohydrates (Produce 4 kcal/g)• : RDA 50% to 60% of total calories/day• Saccharides: simple and complex carbohydrates, fiber

– Mono (glucose, fructose, & galactose): simplest unit– Di (sucrose, lactose, maltose): two monos + water– Poly (glycogen): many units “complex” & also contains fiber

• Fiber– Type I; Insoluble: Not soluble in water

bulk in roughage, cant be used as fuel..– Type II; Soluble: Soluble in water

• Proteins (Produce 4 kcal/g)– RDA 0.8g/kg of body weight per day– Proteins are hard on kidneys; Watch on people w kidney failure– Essential for growth, maintenance, and repair of body tissue– Plays role is transporting drugs systemically– Made of protein; Collagen, hormones, enzymes, immune cells, DNA, and RNA are all made of

protein – breals down into Amino acids; essential and nonessential

– Essential: Body cannot synthesize– Nonessential: Body can synthesize

– Complete and complementary proteins– Complete: Contains enough quantity of amino acids to support growth & maintain a +

nitrogen balance– Incomplete: Missing 1 or more of essential amino acids– Complementary: Pairs of incomplete proteins that = complete when combined

• Simple: Contain only amino acids Ex: Insulin and albumin

• Complex: Protein combined w/ non-protein Lipoprotein = lipid + protein

– Nitrogen balance– Can provide enery, but body uses carbs first

• Fats – Recommended Daily Allowances (RDA)

Fats: 30% of total calories/day No more than 10% of saturated

– Produce 9 kcal/g– Triglycerides and fatty acids– Saturated or unsaturated; monounsaturated or polyunsaturated fatty acids

• Saturated: Each carbon in chain has 2 hydrogen atoms• Unsaturated: Unequal # of hydrogen atoms have 2 or more double carbon bond• Polyunsaturated: Two or more double carbon bonds

– Essential or nonessential fatty acids• Essential fatty acids: Linoleic acid (only one in humans)• Nonessential fatty acids: Linolenic and arachidonic acids (if linoleic acid also available

Linoleic Lowers cholesterol• Water

• Comprises 60% to 70% of body weight• Cell function depends on a fluid environment• Produced during digestion as food is oxidized• Every 100 cal ur body breaks down ur body produces water..Water Loss

– Sensible: Measurable Primarily via kidneys

– Insensible: Immeasurable Respiration Perspiration (normal) Defecation (normal)

• Vitamins and mineralsVitamins

Essential to normal metabolism, As you age you body's need for vitamins stays the same

• Fat-soluble: A, D, E, K• Water-soluble: C and B complexMinerals• Inorganic elements essential as catalysts in biochemical reactions• Macrominerals, dailt need s for these are > or = 100mg

Microminerals or trace elements ; 100 mg or < a day

Metabolism of Nutrients Energy produced by metabolism reserves

• Fat: Adipose tissue• Protein: Muscle mass• Glycogen: Liver

Anabolism: Building of more complex biochemical substances by synthesis of nutrients Catabolism: Breakdown/decomposition of biochemical substances into simpler substances

– Glycogen: Stored in liver & muscle tissue– Glyconeogenesis: Catabolism of amino acids and glycerol into glucose– Glycogenesis: Anabolism of glucose into glycogen for storage– Glycogenolysis: Catabolism of glycogen into glucose, CO2, and H2O

Food Labels• RDIs: Referenced daily intakes• Proteins, vitamins, and minerals• DRVs: Daily referenced values• Total & saturated fats, choles, carbs • fiber, sodium and potassium• Both sets of values: Food labels

Nutritional Needs throughout Growth and Development• Infants through school-age

– Breast-feeding– Formulas– Solid foods– Food habits

• Adolescents– Eating disorders

• Anorexia nervosa: Self imposed starvation they refuse to eat … 85% OF THEIR boy weight or less..have distorted images of them selves… the longer it goes on the more difficult it is to treat.. can go without period for 3-4 months

• Bulimia Nervosa: Binge eating w/ attempts to “lose” what was consumed; excessive exercise, laxatives, diuretics, etc.(Typically will be seen in psych units, but may be undiagnosed and admitted to acute care unit for deterioration of health related to disorders.)

– Activities• Young and middle adults

– Pregnancy– Lactation

• Older adults

Alternative Food PatternsCusterd, hm cooked cereial s.. /…On a soft diet you can have more solid foods, but just depends on how their prepared.,, Low fiber.. Divreticulitus Low sodium...< 2000.. renal diets .. < protien K, Na restrictions

PPN & TPN• Uses: When client is unable to eat and enteral feedings are contraindicated• PPN: Peripheral parenteral nutrition• TPN: Total parenteral nutrition (central parential nutriotion)

Concentration of ing.are greater than 10 % dextrose or greater 5% amino, it has to gevin in a central lineTechnical complications

pnemo thorax, peforate vesssle.. Air embolisism, catheters can become acluted. Or thrombus at site• Septic complications• Metabolic complications

Malnutrition 3 questionsMalnutrition: State of imbalance or deficiency in necessary nutrients

• Primary deficiency: Lack of essential nutrient in the diet– Restrictive Diets:

Reduced calorie (NPO, clear liquids, etc) Reduced intake of particular nutrient (vegan, etc)

– Socioeconomic Status: Lack of available food source Lack of transportation to food source No funds to buy nutritional foods

– Knowledge Deficit: Lacking nutritional info

– Mental Health Issues: Depression

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Anorexia Nervosa Bulimia

– Hospitalized Clients: Anorexia; meds, illness, treatments, etc

• Secondary deficiency: Barriers to use of nutrients once they are consumed– Malabsorption conditions:

Post gastrectomy – Bariatric surgeries– Removal of tumors, CA, fistulas– Traumas– Radiation enteritis– 20 to inflammatory bowel dz

Inflammatory Bowel Disease– Crohn’s disease: Affects any part of intestinal tract, chronic, may affect entire intestinal

wall; May damage tissue thru the intestinal wall, leading to the development of fistulas, fibrosis, strictures, narrowing of the lumen of the bowed (thickening of the intestinal wall)

– Ulcerative colitis: Affects only colon & rectum, acute, limited to submucosal and mucosal

layers only; Most common symptom is bleeding– Both autoimmune disorders

– Other Malabsorption conditions: Biliary diseases Genetic disorders Medication response

Enzyme Disorders Just know how important the enzymes are

Lack of enzymes or genetic disorders:– Celiac’s disease: (gluten-sensitive enteropathy) unable to process gluten; gluten molecules

react with antibiodies in the small intestines causing the villi and the microvilli to flatten out, thereby reducing the surface to absorb nutrients. Recently developed home testing method to test the food for gluten content.

– Cystic Fibrosis: lack of pancreatic ; mucous blocks and damages pancreatic ducts/tissues– Tay-Sachs Disease: (Ashkenazi Jews) do not produce lipid processing enzyme– Lactose intolerance: lack of lactase

Medication Responses May alter lining of intestine or stomach May alter fluid and electrolyte balance May cause anorexia May alter taste of food

Most hospitalized clients!!

Crohn’s Disease Ulcerative Colitis

Hypermetabolic … an abnormally increased rate of metabolism, as in a high fever or hyperthyroidism.

Increases needs

Cancer Cachexia Protein energy malnutrition Clinical Manifestations:

– Progressive weight loss– Anorexia– Generalized muscle wasting– Immunosuppression – Altered BMR

Nursing Goals Prevent or reverse nutrient deficiencies Preserve lean body mass Minimize nutrition related adverse effects Maximize the quality of life

Nursing Care Assist with meals Offer smaller, more frequent meals Treat nausea/diarrhea promptly(side affect of the treatment)

nausea– Elevate HOB after meals– Cool or room temp foods– No high fat, greasy foods– Small, frequent meals– Start SLOWLY, advance AS TOLERATED

Hypermetabolic States

Illness/Fever HyperthyroidismInjury SepsisBurns PainSurgery AgitationCancerAIDS

– Medicate as needed Diarrhea– Low fiber diet (until resolves)– Limit caffeine– Avoid gas producing foods– Limit lactose containing foods– Replace fluid/electrolyte losses

Drug therapy: Megace or Marinol Oral care

Mouth or Throat Problems– Soft and moist foods– No spicy, hot, acidic foods– Avoid extremes in food temperature– Offer nutrient dense foods

Skin care Ensure pleasant eating environment Supplements as ordered

Constipation Increase fluids Increase dietary fiber Encourage mobility Meds….laxatives/stool softners

Fatigue Smaller, more frequent meals Ensure adequate rest Avoid excessive stress Support oxygen needs, watch sats Offer assistance, set up tray

Diabetes; 10 questionsChronic condition: Requires management and treatment on ongoing basis, requires commitment from client to be successfully managedComplications: May lead to heart disease, PVD, stroke, renal failure, blindness, impaired wound healing, neuropathy, orthostatic hypotension, impotence, gastroparesis, neurogenic bladder, impaired visceral pain sensation and on and on….

Leading cause of: – Adult blindness– End stage renal disease– Non-traumatic lower limb amputations– Risk for cardio deaths 2x to 4x higher– Risk for stroke 2x to 4x higher

Type 1 : 5 to 10% of those diagnosed with diabetes have Type 1. Previously called IDDM. Usually diagnosed in childhood or adolescence. Clinical Manifestations

– Presents with symptoms (3P’s)– Typically sudden onset

*** The Three P’s ***– Polydipsia: Excessive thirst

– Polyuria: Excessive urination– Polyphagia: Excessive hunger– Sudden weight loss

Diagnosis Criteria – Causal plasma glucose >200mg/dl ( Causal : Refers to any time of day without regard for last meal)

OR– Fasting plasma glucose >/= 126mg/dl & confirmed by repeat on another day + 3 P(s) is preferred

methodOR

– 2 hour plasma glucose >/= 200mg/dl during OGTT (Oral Glucose Tolerance Test; glucose load of 75 grams of anhydrous glucose dissolved in water. Glucose is checked 2 hours after ingestion ;PREFERRED: FPG )

Type 1 Patho Damage to beta cells of pancreas Thought to be result of autoimmune response caused by:

– Genetic predisposition• Viral infections

– Environmental stimuli• Unknown stimuli

Islet cell autoantibodies are presentWhen the beta cells are damaged, they do not produce adequate insulin. Insulin is the hormone than actually gets glucose into the cells where it can be used as energy. When there is inadequate supply of insulin, the cells begin to starve. The response of the body is to send hunger signals causing the polyphagia. As they eat, the glucose levels build up in the blood (because they can’t get into the cells like they are supposed to) and blood becomes hypertonic. The body responds by trying to rid itself of the excessive glucose in the blood by increasing urine output (polyuria). The resulting “dumping” out of urine causes a third response of thirst (polydipsia).

Insulin a naturally occurring polypeptide hormoneAll type 1 require exogenous insulin. Exogenous is produced outside the body, endogenous is produced by the body. Adults usually secrete 40 to 50 units a day or 0.6 units/Kg of body weight.Goal of insulin therapy is to mimic physiologic insulin therapy

Management of Type 1Type 1 Intensive therapy

Insulin may be given by injection or via pump with dosages adjusted according to results of self monitoring of glucose. At Covenant monitoring is called Accudata. – Admin of insulin > 3x day– Self monitoring >/= 4X day– Dietary intake– Anticipate exercise

Conventional therapy:– Admin of insulin 1-2x day– Self monitoring of urine or blood glucose 1x day– Client education on diet & exercise

Exercise for type 1 Metabolic Control:

– No exercise if glucose > 250 and ketosis present,

– No exercise if glucose> 300 with or without ketosis– Extra carbs if glucose < 100, can exercise, but load up on carbs first

Monitoring: Monitor before and after, client should keep exercise, glu, & food diary to find best time for exercise and how to manageFood Intake: Increase added carbs to prevent hypoglycemia

ketonesAbnormal accumulation of ketones in the body caused by excessive breakdown of fatty acidsDevelops in the absence of adequate metabolism of carbs…as in diabetes Type I

Type 2: 90% of those diagnosed with diabetes have Type 2. Previously called NIDDM. Body produces insulin, but cells do not respond to the insulin produced by the body. Diagnosis Criteria

Adults: 2 hr plasma glucose >/= 200mg/dl during OGTT (or any other tests as for Type I)Children: Overweight AND any 2 of following:1. Family history of type 2 in 10 or 20 relative2. Native American, African American, Hispanic American, Asian-American/Pacific Islander3. Signs of insulin resistance or conditions associated w/ insulin resistance; acanthosis nigricans, HTN, dyslipidemia, or PCOS

Clinical Manifestations Gradual onset of polyuria Gradual onset of polydipsia Easily fatigued Frequent infections (esp UTIs) Often discovered w/ diagnosis of co-morbidity

– co-morbidity often caused by the undiagnosed diabetes. Vision problems, wounds that won’t heal, heart attack, stroke, neuropathies, etc. Many times the clinical manifestations go without notice and it is not until another problem develops that the diagnosis is made.

– Gestation: Pregnancy induced– IGT: Borderline diabetes, most will become diabetic within 10 years

MODY Maturity onset diabetes of the young, Type 2 Diabetes Mellitus #s have tripled in past 20 yrs Obesity #1 risk factor for type 2 diabetes in children Girls more susceptible than boys (ratio is 1.7 to 1)Other clinical signs of MODY are: Polycystic ovarian syndrome; assoc w/ insulin resistance Hypertension (yes, even in children!) Acanthosis nigricans: hyperpigmentation and thickening of the skin into soft, velvety fold around the neck

and flexural areas.

Patho Insulin resistance: Cells do not accept insulin; increased resistance r/t altered cellular metabolism &

intracellular postreceptor defect Insulin secretory defect: Insulin secretion may be normal or decreased Islet cell antibodies: Not present

Cellular resistance is a factor for 60% to 80% of individuals with type 2 diabetes. Insulin resistance is increased with obesity. Decreased beta cell responsiveness to plasma glucose levels is noted, along with abnormal glucagon secretion. The islet dysfunction may be caused by a decrease in beta cell mass, abnormal function of the beta cells, alterations in the insulin receptor, or postreceptor events.46 Levels of insulin may increase (hyperinsulinemia) to compensate for insulin resistance in peripheral tissues, but there is still a relative deficiency of insulin

Risk Factors Obesity and family history are strongest risk factors

Obesity: Produces insulin resistant state causing beta cells to produce excessive amts of insulin Family history: Genetic component Ethnicity: Higher in some ethnic populations

Management Oral agents : Glucose lowering medications; Covered in pharmocology E xercise : Goal time is when glu levels are between 100mg/dl and 200mg/dl OR about 30 to 60 minutes

after meals; Should not exercise when glucose is >250mg/dl & ketones present in urine. Insulin: If criteria met, may use insulin Diet : Nutritionally adequate; spaced throughout day, reduction in total fat intake

Criteria for Use of Insulin Considerations by physician:

Severity of diabetes : degree of hyperglycemia and presence of physical symptoms Comorbidities : Severity of other diseases may make non insulin options less successful Client: Preference / compliance & motivation

Use this to study with!!

AssessmentPhysical exam should include all the usual things and also check for neuropathy, retinopathy, nephropathy, slower wound healiong , and skin break down etc. .

Manage for risks: Clinical manifestations = signs and symptoms; used synonymously.Manage for risks means to be aware of the potential complications of the hospitalized client who has diabetes, they are at greater risk for infection, skin breakdown, altered LOC if glu off, and many other problems.

Attention to skin care Glucose monitoring as ordered and prn Prompt treatment w/ meds Know clinical manifestations of hyper/hypoglycemia

– Hypo: Below normal levels– S/S: Hunger, erratic behavior, confusion, trembling, shaking, cool & clammy skin, pale skin tone

Hypo: May also be called insulin shock or insulin reaction if receiving exogenous insulin. May not have eaten enough with dosage or may be vomiting, may be NPO for test, etc. May have taken or been given wrong dose of insulin.

– Hyper: Above normal levels– S/S: Polyuria, polydipsia, headache

Hyper: May not have taken enough insulin for amount of food ingested. Illness, stress and many other factors may cause increases also.

– DKA: Life threatenin• . If glucose cannot be used by cells ( no insulin to transport) the body breaks down fats and

proteins for energy which may lead to ketosis which is an accumulation of ketones. Glucose builds up in the blood because it can’t get to where it needs to go, so the increased osmotic pressure leads to osmotic diuresis which leads to dehydration. Lactic acid builds up causing lactic acidosis. The pH is lowered from the acidosis which stimulates the respiratory center stimulating deep, rapid respirations AKA Kussmaul’s respirations. Clinical symptoms include fruity or acetone smell to breath, polyuria, polydipsia, vomiting, weakness, fatigue, flushed dry skin, & dry mucous membranes.

Client education r/t all txs, meds, diet, activity, risks, ss of hyper/hypoglycemia CONTROL, CONTROL, CONTROL!!!Treatment of “known” problems:Care of diabetic patient: Should monitor every inch of their skin. Persons with diabetes may have neuropathies that prevent them from having normal pain sensations, esp in the feet.

Skin care for any breakdown & to prevent breakdown Medicate scheduled meds Diet as ordered Treatment/monitoring of comorbidities Reinforce education at every opportunity Treat hypo/hyperglycemia prn

AGAIN…CONTROLTeach clients to:

Have podiatrist trim toenails Monitor temp of bath water Wear protective footwear at all times See physician immediately for any sore that does not heal quickly Recognize s/s of hypo & hyperglycemia Importance of compliance with tx regimen

EvaluationHow frequent are symptoms, how well are symptoms managed as they present, how stable is glucose, how compliant is the client, etc. Evaluation in a chronic condition is ongoing, assess, plan, implement, evaluate and then start all over again!!

Management is key…diabetes is a chronic condition (hemoglobin A1C) looks at glucose levels over a periiod of tiem

Evaluation is ongoing with any chronic condition

Robert is a 34 year old man with Type 1 DM diagnosed 12 years age. His glucose on admission to the hospital is 456mg/dl. His BUN and creatinine are slightly elevated. His white cell count is also elevated. His wife states he has begun to have vision problems and she is not sure he is seeing well enough to administer his own insulin. He states his wife cooks their meals at home and she agrees that he is compliant with the recommended diet.

What is the nurse’s first priority in caring for this man? Treating the hyperglycemiaWhat additional information does the nurse need to develop a POC for this gentleman? Full & recent health history; any recent illness, fever, stress. Any lifestyle changes? Any recent changes in meds?What consultations will the nurse recommend for this client? Dietician, request diabetic educator, request ophthalmologist. Which labs indicate his renal function is abnormal? BUN and Creatinine What might the nurse anticipate precipitated this admission and the elevated glucose level? Infection, illness

Obesity; 3