Patho/Pharm Module 4

Nutrition/Vitamins/CAM

CAM safety - patient responsibilities

consult with provider before, report what you are taking to provider, inform provider of allergy or sensitivities, use caution if pregnant or lactating, don’t take a greater dose than recommended

Dietary Supplement Health and Education Act of 1994 (DSHEA)

must be on label:

1. name of the supplement

2. amount of supplement

3. nutrition labeling

4. ingredients list

5. name and place of the manufacturer, packer, or distributor

physiologic effects can be noted (e.g. maintains blood flow, promotes health immunity)

no claims can be made about CAMs use in order to diagnose, treat, prevent or cure any disease or specific condition (e.g. lowers blood pressure, cures diabetes)

commonly used herbs

cinnamon, echinacea, garlic, ginger, ginkgo biloba, ginseng, green tea, kava kava, valerian, turmeric, peppermint, licorice root, saw palmetto, St. John’s wort

echinacea

used for colds, flu, infections

stimulates immune system

side effects include GI effects, allergic reactions

garlic

used to lower cholesterol and blood pressure and reduce heart disease, preventing stomach and color cancer

side effects: heartburn/upset stomach, body odor, decreased blood clotting time

ginkgo biloba

used for asthma, bronchitis, fatigue, tinnitus

used to improve memory, prevent Alzheimer disease

decrease intermittent claudication

treats sexual dysfunction, multiple sclerosis

side effects headache and dizziness, GI upset/nausea, increased bleeding, allergic reactions

ginseng

improves well-being, stamina, and immune system

treats erectile dysfunction, hepatitis C, menopausal symptoms

lowers blood glucose and blood pressure

side effects: headaches, GI distress, hypertension, hypoglycemia, breast tenderness, menstrual irregularities, allergic reactions

St. John’s wort

used for mental disorders, nerve pain

side effects: anxiety, dizziness, headache, fatigue, sensitivity to sunlight, GI problems, sexual dysfunction, many drug interactions

potential hazards of herbs

natural substances does not mean safe

herb-drug interactions are possible

herbal products can affect lab results

not all compounds are safe via all routes

many products may interfere with absorption, breakdown, and excretion of anesthetics, anticoagulants, and other drugs used in surgery

discontinue herbal therapy 2 to 3 weeks before surgery

digestive processes

1. ingestions and breakdown of food

2. propulsion of food and wastes from the mouth to the anus

3. secretion of mucus, water, and enzymes

4. mechanical digestion of food particles

5. chemical digestion of food particles

6. absorption of digested food and fluid

7. elimination of wastes by defecation

8. immune and microbial protection against infection

anatomy of the digestive system

internal digestion and absorption

from stomach to duodenum:

• gastric HCL and pepsin begin protein digestion

• food is converted to chyme

• chyme enters the duodenum (proximal small intestine) containing:

  • partially digested carbohydrates

  • partially digested proteins

  • partially digested fats

• further digestion is required in the small intestine

carbohydrate digestion in the SI

pancreatic amylase and brush border enzymes

broken down into absorbable “simple” sugars

disorders affecting the liver or portal circulation may impair carbohydrate metabolism

protein digestion in the SI

pancreatic proteases and intestinal peptidases

broken down into amino acids and small peptides

malabsorption of proteins can lead to edema, muscle wasting, and poor wound healing

fat digestion in the SI

bile salts emulsify fats

pancreatic lipase produces fatty acids and monoglycerides

pale, greasy stools (steatorrhea) suggest impaired fat absorption

nutrient absorption pathways

carbohydrates and proteins → villus capillaries → hepatic portal vein → liver (stored or used)

fats → lacteals (lymph vessels) → lymph → systemic circulation (stored or used)

diseases that can severely impair digestion

diseases affecting the pancreas, liver, or bile ducts

obesity causes

interaction of brain, hormones and neurotransmitters, and adipose tissue

occurs when energy intake > energy expenditure in genetically susceptible people

3 leading causes of death

cardiovascular disease

type 2 diabetes mellitus

cancer

*all associated with obesity

obesity risk factors

genetic defects

gene-environment interactions

metabolic abnormalities

environmental factors

depression and mood disorders

adipocytes

basis of obesity

with excess calories: fat cells grow larger (hypertrophy), new fat cells form (hyperplasia/adipogenesis), fat is stored as triglycerides

adipokines

signaling hormones released be fat cells

circulate in the blood

increase with greater fat mass

signal the brain to regulate: hunger, satiety, and energy balance

also affect: insulin sensitivity, inflammation, blood pressure, and vascular health

chronic obesity

produces a state of chronic, low-grade inflammation

key hormone changes: promotes inflammation, reduces anti-inflammatory protection, increases insulin resistance

chronic inflammation leads to: insulin resistance, metabolic syndrome, alterations in intestinal microbiome

obesity increases risk for:

type 2 diabetes mellitus

cardiovascular disease

kidney disease

nonalcoholic steatohepatitis (NASH)

cancer

obesity treatment

lifestyle changes (diet and exercise)

behavioral therapy and support systems

medications for weight loss

bariatric surgery (greatest improvement): Roux-en-Y gastric bypass, adjustable gastric banding, sleeve gastrectomy

malnutrition and obesity

common in low-income populations

may have micronutrient deficiencies or over-nutrition

often due to excess intake of low-quality, nutrient-poor foods

short-term starvation

extended fasting, several days of dietary abstinence or deprivation

therapeutic: initial rapid weight loss

body responds to protect protein mass - glycogenolysis, gluconeogenesis

used in some weight-loss programs

may increase motivation to diet

long-term starvation

begins after several days of dietary abstinence

therapeutic: weight loss in morbidly obese people

pathologic: harmful and uncontrolled, poverty or food shortages, chronic disease, malabsorption syndromes, HIV infection, cancer, eating disorders

causes death from proteolysis

marasmus

total calorie deficiency

skin and bones appearance

sunken abdomen

no hepatomegaly

skin is thin and wrinkled

sparse, thin hair

marasmic kwashiorkor

chronic energy deficiency

chronic or acute protein deficiency

inadequate micronutrients

edematous

severe childhood malnutrition

kwashiokor

protein deprivation with carbohydrate intake

generalized edema

almost normal weight for age

abdominal distention

fatty liver

skin is dry, shiny, patchy pigmentation

hair is brittle, color changes

refeeding syndrome

life threatening condition when nutrition is restarted too quickly in a malnourished patient

causes rapid shifts in fluid and electrolytes: low levels of phosphate, potassium, magnesium

cardiovascular, neurological, respiratory symptoms

monitor electrolytes closely and reintroduce nutrition slowly and safely

anorexia of aging

decreased appetite and food intake in older adults

common but not a normal part of aging

often linked to a chronic disease progression

anorexia of aging risk factors

functional impairments (loss of vision, poor dentition, dysphagia, unable to prepare foods)

medical and psychiatric conditions

loneliness and grief

social isolation

medications and polycharmacy

abuse or neglect

anorexia of aging consequences

malnutrition

physical frailty and weakness

muscle and mitochondrial dysfunction

decreased ability to regenerate tissue

increased oxidative stress

hormonal imbalance

higher mortality rates, especially with unintentional weight loss

anorexia of aging management

early intervention improves outcomes

no single specific treatment

supportive strategies: exercise (improves appetite, mood, muscle strength), adequate nutrition support, improved food access and presentation, dental and eye care, social stimulation

clef lip and cleft palate

congenital separation of the lip and/or palate from incomplete fetal fusion

cleft lip and cleft palate risks/complication

increased ear infections

difficulty swallowing, aspiration

feeding problems

speech delays

assessment cues: visible gap, poor suction, nasal regurgitation during feeds

feeding support: upright positioning, specialized bottles, frequent burping

cleft lip and cleft palate treatment

surgical repair: lip repair around 3 months, palate repair around 6-12 months

post-op priorities: protect incision (no suction devices), manage pain, maintain airway, prevent infection

follow-up needs: speech therapy, hearing monitoring, dental/ENT involvement

infantile hypertrophic pyloric stenosis

acquired narrowing and distal obstruction of the pylorus

unknown etiology

forceful, non-bilious vomiting immediately after feeding starting 2-3 weeks after birth

vomiting causes weight loss, electrolyte imbalances, and dehydration

infant irritable as a result of hunger and esphageal discomfort

infantile hypertrophic pyloric stenosis evaluation and treatment

hypertrophic pylorus is palpable in the RUQ

standard treatment is pyloromyotomy

pre- and post-op medical management to correct fluid and electrolyte imbalance (key to high success and low complication rates)

duodenal obstruction

upper abdominal distention, visible peristaltic waves, decrease in meconium stools

weight loss

persistent vomiting

dehydration

obstruction may be partial to complete

“double bubble” sign on imaging

acquired impairment of GI motility

gastroesophageal reflux (GER): normal, physiologic reflux, common in infants, self-resolving

gastroesophageal reflux disease (GERD): pathologic reflux = symptoms or complications affecting function

GER/GERD pathophysiology

transient lower esophageal sphincter relaxation

GER/GERD contributing factors

decreased LES tone

impaired esophageal clearance

acidic reflux leads to esophagitis and vomiting reflex

high risk populations: prematurity, neurologic impairment, obesity, CF, hiatal hernia

GER/GERD clinical cues

irritability, arching, regurgitation, poor growth and weight loss, hematemesis

extra-esophageal signs: cough, wheeze, otitis media, laryngitis

diagnosis is often clinical

GER/GERD nursing interventions

monitor growth, feeding tolerance, and respiratory symptoms

educate caregiver on proper feeding techniques

identify complications

GERD complications

poor growth, weight loss, dehydration, or persistent feeding refusal

GI bleeding: hematemesis, melena, or anemia

severe/persistent vomiting, bilious, or forceful emesis

significant pain

respiratory compromise: apnea, cyanosis, aspiration, chronic cough/wheeze

nursing considerations for kwashiorkor and marasmus

high risk for infection due to immune suppression

early nutritional rehab is critical to prevent irreversible damage

faltering growth

a physical sign that manifests as low weight or BMI over time, decrease in the velocity in weight gain

faltering growth causes

inadequate caloric intake

inadequate caloric absorption

excessive caloric expenditure

faltering growth clinical manifestations

dry skin, sparse hair, poorly defined muscles, decrease SQ fat, abdominal swelling, vitamin deficiencies (Rickets), decreased responsiveness/interactions

diarrhea in infants and children

more than 3 watery or loose stools in 24 hours

usually self-limiting (less than 72 hours)

leading cause of death <5 years of age globally (high risk in preterm infants)

causes of diarrhea in infants and children

infectious diarrhea - rotavirus, norovirus, adenovirus, C-diff

contaminated food or water

lactose intolerance

toxins

clinical cues for diarrhea in infants and children

dehydration = red flag

watery, bloody stools

fever

vomiting, abdominal cramping

management and prevention of diarrhea in infants and children

oral rehydration therapy (ORT) first-line

electrolyte replacement, early nutrition

antibiotics only if pathogen identified

IV fluids only if oral not tolerated

prevention: clean water, hygiene, rotavirus vaccine

smaller fluid reserves increases risk for dehydration

faltering growth (failure to thrive)

nutritional support benefits

provide energy, promote growth and development, regulate body processes, restores intestinal motility, maintains GI function, reduces movement of bacteria, improves wound healing, decreases incidence of infection, decreases length of hospital stay, improves general health

nutritional support factors to consider

patient’s condition, preferences, length of the feeding, physiological conditions, tolerance, integrity of the GI tract

enteral nutrition is always preferred when the GI tract is functional because it is safer, more natural, and has fewer complication

parenteral nutrition is used only when enteral feeding is not possible or contraindicated

oral feeding

patient can swallow and has functioning GI tract

oral nutritional supplements

enteral nutrition

patient may have swallowing difficulties with functioning GI tract

delivers nutrition or fluid via tube into GI tract

routes for enteral nutrition

nasogastric, nasoduodenal/nasojejunal, gastrostomy, jejunostomy

methods for nutrition delivery

continuous infusion pump

intermittent infusion

intermittent bolus by syringe

cyclic method

enteral nutrition support complications

dehydration: diarrhea, high protein/concentrated formulas, may need added fluids to prevent

aspiration pneumonitis: life threatening, always check residual by aspirating gastric contents - before starting and every 4 hours

diarrhea: rapid administration, contaminated formula, drugs

enteral nutritional support safety

proper patient position: elevate HOB 30-45 degrees

check gastric residual: prior to intermittent feedings, Q4-6h if continuous feedings

confirm newly inserted tube before beginning feedings per agency policy - usually by X-ray

check placement before any infusion: auscultate or pH testing

enteral med admin common problems

drug incompatible with administration through a tube

failure to prepare drug properly

use of faulty techniques

always make sure a non-liquid medication is crushable and not an extended release or enteric coated medication

contact the pharmacist and provider if not an appropriate formulation

enteral med admin adverse results

occluded feeding tube

reduced drug effect

drug toxicity

harm

death

nursing implications for enteral medications

ensure drug is crushable

validate with pharmacist that drug dissolves water and can be absorbed enterally

drugs that cannot be dissolved: time-released, enteric coated, sublingual

prepare each medication separately

open capsules separately, dissolve in 15mL water

never mix medications with feeding formula, flush tub before and after medication delivery

total parenteral nutrition indications

bowel obstruction

prolonged paralytic ileus

inflammatory bowel disease

severe pancreatitis

need bowel rest

severe trauma

severely malnourished

parenteral nutrition nutrients

amino acids, carbs, electrolytes, fats, trace elements, vitamins, water

parenteral nutrition complications

pneumothorax, hemothorax, air embolism (prevention: valsalva maneuver), infection (strict aseptic technique), hyperglycemia, hypoglycemia, hypervolemia

inability to metabolize and absorb vitamins deficiencies

malabsorption disorders: diarrhea, infectious and inflammatory disease (e.g. Crohn’s disease, celiac disease)

inability to use vitamins deficiencies

liver disease (cirrhosis, hepatitis), renal disease, certain hereditary deficiencies (cystic fibrosis)

increased vitamin losses deficiencies

fever from infectious processes, hyperthyroidism, hemodialysis, cancer, starvation, crash diets

increased vitamin requirements deficiencies

early childhood, pregnancy, debilitating disease (cancer, alcoholism), gastrointestinal surgery, special diets

fat soluble vitamins

vitamin A

vitamin D

vitamin E

vitamin K

vitamin A (retinol) food sources

beta-cerotene: plant based darkly color fruits/veggies: carrots, cantaloupe, spinach

retinoids: animal origin dairy, meat, fish and fish oil

vitamin A (retinol) function

bone growth

epithelial tissue, skin, eyes, and hair maintenance

vitamin A (retinol) deficiency

night blindness, corneal dryness and ulceration

skin lesions, dysfunction of mucous membranes

vitamin A (retinol) excess doses

teratogenic effect

liver damage

hypervitaminosis A: hair loss, peeling skin, GI upset, lethargy

vitamin D food source

fortified milk, eggs, fatty fish

vitamin D function

regulates calcium and phosphorus metabolism

needed for intestinal calcium absorption (from dietary calcium)

vitamin D deficiency

rickets in children

osteomalacia in adults

bone fractures

vitamin D excess doses

hypervitaminosis D : hypercalcemia, anorexia, nausea, vomiting

vitamin E food source

whole grains, milk eggs, avocados, asparagus, broccoli, veg oils

vitamin E function

protect cellular components from being oxidized

protect RBCs from hemolysis

vitamin E deficiency

breakdown of RBCs

vitamin E excess doses

fatigue, weakness, GI upset

headaches, breast tenderness, bleeding

vitamin E interaction

iron can interfere with absorption and use

vitamin K food source

leafy greens, liver, cheese, egg yolk, veg oils

vitamin K function

needed for synthesis of prothrombin and clotting factors VII, IX, X

antidote for oral anticoagulant warfarin overdose

prevent and treat hypoprothrombinemia

vitamin K deficiency

spontaneous hemorrhage, increased bruising

bleeding from mucous membranes

dark, tarry stools

vitamin K excess doses

blood clot formation, stroke , heart attack

water soluble vitamins

vitamin B

vitamin C

vitamin B1

thiamine

promotes carb metabolism

vitamin B2

riboflavin

promotes use of carbs, proteins, and fats

vitamin B3

nicotinic acid or niacin

needed for energy production

vitamin B6

pyridoxine

required for amino acid, carb, and lipid metabolism, and formation of RBCs

vitamin B9 (folic acid) food sources

green leafy, yellow fruits/veggies, organ meats, black-eyed peas

vitamin B9 (folic acid) function

essential for DNA synthesis

body growth and GI function

vitamin B9 (folic acid) deficiency

GI upset, glossitis, stomatitis, fatigue, alopecia

megaloblastic anemia, leukopenia, thrombocytopenia

neuropsychiatric problems

during pregnancy, can affect fetal CNS development - neural tube defect, prematurity