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Health and Illness > Exam 1 > Flashcards

Exam 1 Flashcards

1
Q

What is the definition of nutrition?

A

The science of optimal cellular metabolism and its impact on health and disease

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2
Q

What is the basal metabolic rate?

A

resting metabolism, what the body needs if at rest

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3
Q

What are the effecting factors for basal metabolic rate? How do they effect BMR?

A

muscle mass: higher muscle mass, high BMR
age: higher age, lower BMR
genetics
weather: higher temperature (fever), higher BMR
diet: several several small meals can increase BMR, starvation will decrease BMR
pregnancy: higher BMR
significant injuries and surgeries: increase BMR

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4
Q

What is the mifflin-st. jeor equation?

A

calculates BMR based on height, weight, age, and activity factor

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5
Q

What are the mifflin-st.jeor for those trying to lose weight, maintain weight, and gain weight?

A

lose = 20 to 25 kcal/kg
maintain = 25 to 30 kcal/kg
gain = 30 to 35 kcal/kg

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6
Q

What are examples of simple vs complex carbohydrates?

A

simple = sugar, white bread, honey
complex = whole grains, potatoes, legumes

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7
Q

What are carbohydrates broken down into?

A

glucose, frutose, galactose

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8
Q

Where are carbohydrates absorbed and moved to?

A

small intestine; liver

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9
Q

What is the job of fiber?

A

keep the GI tract flowing

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10
Q

How much fiber is recommended?

A

14 g per 1000 calories

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11
Q

How much energy do fats provide vs carbohydrates?

A

twice the amount of energy as an equal mass of carbohydrates

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12
Q

What is the purpose of fats?

A

carry essential fatty acids and fat-soluble vitamins

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13
Q

What are examples of potentially harmful vs healthy fats?

A

saturated and trans fats (tropical oils, butter)
monounsaturated and polyunsaturated (plant based oils)

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14
Q

What is the purpose of proteins?

A

maintain and repairs cells to produce enzymes, hormones, other nitrogen compounds the body needs

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15
Q

What are complete vs incomplete proteins and examples?

A

complete contains all essential amino acids (ex/ milk, eggs, poultry)
incomplete lack one or more amino acids (ex/ seeds, nuts, legumes)

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16
Q

How much of the diet should consist of proteins?

A

10 to 25%

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17
Q

What are the water soluble and fat soluble vitamins?

A

water: B,C
fat: ADEK

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18
Q

What is the potential risk associated with fat soluble vitamins?

A

potential for toxicity

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19
Q

What are the major and trace minerals?

A

major: C, Mg, P, Na
trace: Zn, Fe, I

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20
Q

What are the typical daily intake goal for water for men and women?

A

125 oz for men
91 oz for women

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21
Q

What are the components of a nutritional assessment?

A

history: health and diet
physical exam
anthropometric measurements, functional measurements, laboratory tests

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22
Q

What are the antropometric measurements for infants? For adults?

A

length, head circumference; height, weight, BMI, skinfold thickness, mid-arm muscle circumference, waist circumference, hip-to-waist ratio

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23
Q

What are functional measurements? Examples?

A

ability to perform basic and instrumental activities of daily living; Katz index looks at ADLs and Lawton scale looks at the independence of chores, finances, upkeep of self and household, hand grip strength, performance tests (Get up and go)

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24
Q

Is serum albumin a good predictor of malnutrition?

A

no, it is impacted by a lot of other factors and lags behind protein intake by about 2 weeks

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25
Q

Which laboratory tests can be used to review nutrition of a patient?

A

prealbumin, blood glucose, lipid profile (total cholesterol, LDL, HDL, triglycerides), electrolytes (for micronutrients), hemoglobin and hematocrit

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26
Q

What could a high hematocrit indicate? A low hematocrit indicates?

A

dehydration
anemia

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27
Q

What is the pathophysiology of GERD?

A

movement of the stomach acid into the lower esophagus due to a dysfunctional lower esophageal sphincter

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28
Q

Who can GERD affect?

A

anyone from babies to adults, but babies can outgrow GERD as the GI is still developing

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29
Q

Why can GERD be often misdiagnosed or a diagnosis be delayed?

A

symptoms are mild to go into a clinic or are misinterpreted

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30
Q

What causes GERD?

A

the exact cause is unknown but the dysfunction of the LES could be due to transient relaxation or complete incompetence

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31
Q

What are risk factors of GERD? Examples?

A

lifestyle (alcohol and cigarette)
medications (reduce tone of LES, calcium channel blockers and anticholinergics)
diet (fatty, fried, garlic, onions, caffeine, citrus foods, tomatoes, spicy)
eating habits (eating large meals cause gastric distension and LES weakening, laying down right after eating, eating right before bedtime)
other medical conditions (increase intrabdominal pressure and weaken LES, hiatal hernia, pregnancy, obesity)

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32
Q

What are the clinical manifestations of GERD?

A

vary mild to severe, pyrosis (heart burn that can spread from chest to throat and cause a sour taste in the mouth), dyspepsia (pain or discomfort midline in abdomen), dysphagia, regurgitation of food our sour liquid (acid reflex), respiratory symptoms (wheezing, cough, dyspnea, mimics asthma), otolaryngologic (hoarseness or sore throat, feel a lump in the throat), atypical chest pain (mimics angina but will be relieved with antiacids)

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33
Q

How is GERD diagnosed?

A

symptoms and predisposing factors, suspected GERD patient may have lifestyle modifications and a trial OTC medication and if this does not work then a diagnostic test may be performed

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34
Q

What is the gold standard GERD diagnostic test? What does it do?

A

upper GI and endoscopy with biopsy and cytologic analysis; assesses function of LES and the degree of inflammation present, scarring, strictures, a biopsy looks for stomach or esophageal cancer

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35
Q

What are diagnostic tests for GERD? What do they look at?

A

esophagram (ability to swallow), motility (manometry) studies (looks at pressure of esophagus and LES), pH monitoring of stomach, radionucleotide studies (small amount of radioactive material injected and then the body is scanned looking for reflux of gastric contents and rate of esophageal clearance)

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36
Q

What is an esophageal stricture?

A

complication of GERD, narrowing of esophagus due to damage and development of scar tissue, can also lead to dysphagia

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37
Q

What is Barrett’s esophagus?

A

complication of GERD, patches of red tissue amongst normal tissue that is a pre-cancerous lesion, increase risk of esophageal cancer, if present patient will be recommended an endoscopy every two to three years to monitor lesions

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38
Q

What can an esophageal ulcer lead to?

A

bleeding and increased inflammation

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39
Q

What are some non-medication treatments for GERD?

A

lifestyle modifications, nutritional therapy and dietary changes (food log to determine which foods could trigger GERD, eat smaller meals, not eating before bedtime), surgery to reinforce the LES (labaroscopic nissen fundoplication)

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40
Q

What are some medications to treat GERD?

A

antacids, H2 receptor antagonists, proton pump inhibitors

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41
Q

What are antacids? MOA? Considerations? Interactions?

A

used for GERD (not super effective for chronic GERD as it doesn’t heal lesions) OTC: Al, Ca, Mg, or Na salts; neutralize acid (raise stomach pH by 0.1) and stimulate stomach mucosa; should take 1 to 3 hours after eating, chronic usage throughout the day could be an indication of a bigger problem that is undiagnosed (severe reflux or ulcers, gallbladder issues); Mg can cause diarrhea and cannot be used in those with renal failure, Ca if overused can cause kidney stones and hypercalcemia, cannot be taken with quinolones as can cause chelation and decrease absorption of the antibiotic by half (therefore should take antibiotic two hours before or after taking antacid)

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42
Q

What is famotidine and cimetidine? MOA? Side effects?

A

H2 receptor antagonists that can help GERD or when used with other medications can control upper GI bleeds; blocks H2 receptors of acid producing parietal cells to reduce acid secretion; headaches, diarrhea, fatigue, rare CNA adverse effects in elderly (confusion, disorientation), if taken long term can change pH of stomach and effect absorption of medications, if taken with antacids should be taken 2 hours before antacids

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43
Q

What is lansoprazole, omeprazole, pantoprazole, and esomeprazole? MOA? Nursing considerations?

A

proton pump inhibitors; binds to hydrogen-potassium-ATPase pump to block all acid secretion from parietal cells; well tolerated, can be taken daily, long term use can increase risk for osteoporosis and fractures, take on an empty stomach 30 to 60 minutes before eating, can lead to toxicity of diazepam, phenotine (seizures), and warfarin

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44
Q

What are some nursing education points for GERD?

A

avoid foods that cause reflux, frequent small meals, avoid laying down after meals, sleep with HOB elevated, instructions on drug usage, weight loss

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45
Q

What are malabsorption disorders?

A

impaired or insufficient absorption of either micronutrients or macronutrients or both due to inefficient intestinal mucosa

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46
Q

What are examples of malabsorption disorders?

A

lactose intolerance, celiac disease, short bowel syndrome, tropical sprue, cystic fibrosis

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47
Q

How is celiac disease transmitted? Who is at risk?

A

it is hereditary, those with a first degree relative with celiac (parent, child, or sibling) have a 1 in 10 chance for developing the disease

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48
Q

What is the pathophysiology of celiac disease?

A

autoimmune disease that can develop at any age after people start eating foods or medications that contains gluten, wheat, barley, and rye cause an immune response which will damage the small intestine mucosa and villi

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49
Q

What are the symptoms of celiac disease?

A

abdominal bloating and pain, chronic diarrhea, vomiting, constipation, steatorrhea (foul-smelling, fatty stool), weight loss, failure to thrive, fatigue, behavioral issues, dental enamel defects, delayed growth and puberty

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50
Q

What is the gold standard diagnostic test for celiac disease?

A

tissue biopsy to see flattened mucosa and loss of villi

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51
Q

What are diagnostic tests for celiac disease?

A

patient goes entirely gluten free and symptoms cease, lab tests for antibodies before starting a gluten free diet

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52
Q

What is the treatment for celiac disease?

A

the only treatment is lifelong adherence to a strict gluten-free diet, vitamin and mineral supplements, iron and folic acid for anemia, vitamin K, corticosteroids for inflammation if diet does not help completely

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53
Q

What are some long term health effects of celiac disease?

A

if left untreated can lead to serious health problems: type 1 diabetes, RA, thyroid disease, dermatitis herpetiformis (itchy red rash on face, butt, knees, elbows, or scalp), anemia, osteoporosis, infertility and miscarriage, epilepsy, migraines, intestinal cancers

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54
Q

What causes lactase deficiency? How is it transmitted?

A

lactase enzyme is deficient or absent; genetics

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55
Q

What are symptoms of lactase deficiency?

A

the following can occur about 30 minutes after eating milk products: bloating, cramping, abdominal pain, flatulence, diarrhea

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56
Q

What diagnostic tests can be done for lactase deficiency?

A

lactose tolerance test (serial testing done before and after drinking a liquid that contains lactase to measure how well the body can process lactose), lactose hydrogen breath test (measures amount of hydrogen exhaled by patient after ingestion of lactose, if deficient hydrogen levels increase), genetic testing

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57
Q

What are some treatments for lactase deficiency?

A

eliminate lactose from diet or for some reintroducing small amounts of lactose, lactase enzyme, calcium supplements (osteoporosis)

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58
Q

What is short bowel syndrome? Causes?

A

not enough surface area of the intestines to allow for adequate absorption; diseases that damage the intestinal mucosa, surgical removal of small intestine, congenital defects

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59
Q

What are symptoms of short bowel syndrome?

A

diarrhea, steatorrhea, malnutrition

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60
Q

What are some non-medicine treatments for short bowel syndrome?

A

high carb, low fat diet, frequent small meals, supplemental feeding, multivitamins, intestinal transplant

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61
Q

What is loperamide?

A

opioid antidiarrheal that will decrease intestinal motility and treat short bowel syndrome

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62
Q

What is teduglutide?

A

increases intestinal mucosa growth to improve intestinal absorption to treat short bowel syndrome

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63
Q

What is somatropin?

A

growth hormone to help treat short bowel syndrome

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64
Q

What is glutamine?

A

improves intestinal absorption to help treat short bowel syndrome

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65
Q

What is malnutrition?

A

imbalance of nutrients ranging from insufficient nutrition to excess nutrition

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66
Q

What are contributing factors to malnutrition?

A

socioeconomic, physical illness, incomplete diets (not a big issue in first world countries due to fortification), incomplete diets, drug-nutrient interactions

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67
Q

Which populations are at risk for undernutrition?

A

infants, children, and adolescents because they are growing and need a lot of calories and nutrients

older people (about half older people in hospitals and LTC facilities do not consume enough calories)

patients admitted to the hospital

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68
Q

What factors contribute to older people malnutrition?

A

changes in appetite/problems chewing or swallowing, limited income, social isolation, functional limitations, limited transportation, chronic illness (depression, dementia, dysphagia, oral health, medications)

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69
Q

What is the pathophysiology of starvation?

A

stage 1: liver and muscle glycogenolysis (occurs in less than a day)
stage 2: gluconeogenesis (occurs within 5 to 9 days and will last around 4 to 6 weeks)
stage 3: terminal, protein degradation

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70
Q

What are the overall effects of starvation?

A

pancreas reduces insulin secretions, metabolic rate is decreased, many organs begin to shrink, villi shrink decreasing the ability to absorb nutrients, if untreated will lead to mental or physical disability, illness, and death

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71
Q

What usually the cause of death from starvation?

A

infection due to impaired immune system

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72
Q

What are the clinical manifestations of starvation?

A

decreased immunity, delayed wound healing, skin/hair changes, brittle/malformed nails, decreased muscle tone, mouth changes, mental status changes, amenorrhea, decrease in all lab values

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73
Q

What are indications for nutritional supplementation?

A

unable to take any oral intake for more than 5 days, critical illness requiring mechanical ventilation, hypermetabolic states (trauma, fever), severe physical stress (infection, burns, major surgery, chemo or radiation therapy), malabsorption caused by disorders (pancreatitis) or wounds

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74
Q

What is hyperalimentation?

A

type of parenteral nutrition that contains 20 to 50% (hypertonic) is glucose, also contains protein hydrolysates, minerals, and vitamins

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75
Q

What is lipid emulsions?

A

type of parenteral nutrition that contains essential fatty acids and energy-dense calories such as soybean or safflower triglycerides

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76
Q

How can parenteral nutrition be administered?

A

peripheral (into larger vein for short period of time and not a high caloric need), central lines (longer term and higher caloric need, ex/ PICC, midline), triple/double/single lumen catheters

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77
Q

What are some nursing considerations for parenteral nutrition?

A

fluid and electrolyte imbalances, line infections (parenteral is thick and sticky), liver and kidney dysfunction, hyper/hypoglycemia, medication incompatibility

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78
Q

How many people in the US have obesity?

A

about 13 million of US children 2 to 19, about 40% of adults (most prevalent preventable health problem in the US)

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79
Q

What are the risk factors for obesity?

A

genetics (study found BMI correlated with children’s birth parents rather than their adoptive parents), environment (quality, quantity of food, portion sizes increased dramatically over time, socioeconomic status), psychosocial factors (mindless eating, social component to food and eating, used for comfort or reward)

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80
Q

What are the types of obesity?

A

primary: excess caloric intake over energy expenditure for body metabolic demands
secondary: from congenital or chromosomal abnormalities, metabolic problems, brain lesions or disorders, more rare

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81
Q

How is appetite regulated?

A

hormones synthesized by the gut and adipose involved in stimulating or inhibiting appetite and regulating obesity, Neuropeptide Y is synthesized by the hypothalamus and stimulate appetite, leptin is synthesized from the adipose and known as the “starvation hormone” targets area of the hypothalamus to inhibit appetite (in obese people this is high due to bodily resistance), ghrelin is synthesized from the gut and inhibits leptin to stimulate appetite (can play a part in compulsive and reward eating, those who undergo a certain gastric bypass surgery will have their ghrelin levels decreased)

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82
Q

What is BMI? Flaws? Standards for normal, overweight, obesity, extreme obesity?

A

measurement of body fat based on height and weight; does not distinguish between fat, muscle, and bone mass;
normal = 18.5-24.9
overweight =25-29.9
obesity greater than or equal to 30
extreme obesity greater than or equal to 40

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83
Q

What does waist circumference measure? What is considered obese in men and women?

A

visceral fat; men greater than 40 inches, women greater than 35 inches

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84
Q

What does waist-to-hip ratio measure? What is considered obese?

A

distribution of SQ and visceral fat; WHR greater than 0.8 indicates more truncal fat

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85
Q

Which labs are looked at for obesity?

A

thyroid panel (link between hypothyroidism and weight gain), blood glucose (obesity is a risk factor for diabetes), lipid panel (obesity is a risk factor for heart disease)

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86
Q

What is the correlation between body shape and obesity?

A

people who carry most of their weight around the waist have a greater risk of heart disease and diabetes than people with big hips and thighs

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87
Q

What are complications of obesity?

A

significant risk for CV disease, 60% have metabolic syndrome, insulin resistance and type 2 DM, reproductive function, gallstones, GERD, cancer, osteoarthritis in weight bearing joints, depression/social discrimination, sleep apnea, chronic lower back pain

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88
Q

What is metabolic syndrome? Criteria for diagnosis?

A

risk factors that can increase a person’s chance of developing CV disease, stroke, and diabetes, seen in about 1 in 3 adults; patient has three or more risk factors: obesity (increased waist circumference), hypertension (BP is greater than 130/85), abnormal lipid levels (elevated triglycerides or low HDL), high blood glucose (greater than 100 fasting glucose)

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89
Q

What are some non-pharmaceutical treatment for obesity?

A

nutrition: create a diet plan with 500-1000kcal deficit, low cal, low fat, high fiber, very low cal diet for those with BMI greater than 30 for a short amount of time

exercise: 30 to 60 min daily which will help speed up metabolism and reduce “set point” to a lower natural weight

behavior modification: stimulus control (ID high risk situations), rewards that are not food related, support

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90
Q

Who can benefit from pharmacological therapies for obesity?

A

adults with BMI greater than thirty or those with BMI greater than 27 and have at least one other weight related risk factor or comorbidity

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91
Q

What is phentermine, diethylpropion, and phendimetrazine?

A

appetite-suppressing drugs that will stimulate the CNS, cannot be used longer than 3 months due to side effects: dizziness, insomnia, constipation, dry mouth, tachycardia

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92
Q

What is orlistat?

A

nutrient absorption-blocking drug for obesity, blocks fat breakdown and absorption in the intestines, side effects include: stool leakage, diarrhea, bloating, flatulence

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93
Q

What is lorcaserin?

A

serotonin agonist for obesity, suppresses appetite and increases satiety by activating serotonin receptors

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94
Q

What is phentermine and topiramate?

A

sympathomimetic and anti-seizure/migraine drug for obesity that will suppress appetite and increase satiety

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95
Q

What are the qualifications for bariatric surgery?

A

BMI of 40 or higher or BMI of 35 or higher with significant co-morbidities

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96
Q

What are some post-op complications for bariatric surgery?

A

leaks, dumping syndrome (RYGB, gastric contents go too fast into intestines and overwhelm body’s ability to digest nutrients), reflux, bowel obstruction, vitamin deficiency, malnutrition, regain weight (stomach stretch to same size), excess skin

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97
Q

What is the difference between dehydration and fluid volume deficit?

A

dehydration is the loss of water alone while fluid volume deficit is the loss of water, electrolytes, and blood

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98
Q

What is fluid spacing?

A

how water is distributed in the body
1st: normal distribution intracellular and extracellular
2nd: interstitial fluid, easy to reverse, close to normal conditions (ex/edema)
3rd: fluid is quite impossible to return to normal without interventions (via needle aspiration)(ex/ ascites)

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99
Q

What are the lifespan considerations for body water?

A

preterm babies: about 80%
newborn: about 75%
adults: about 50 to 60%
older adults 45 to 50%

older adults and preterm babies are at high risk for fluctuations in fluid and electrolytes

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100
Q

Where is most body water located? Where is the rest?

A

intracellularly; extracellular fluid can be found in the plasma, cerebral spinal fluids, GI fluid, ect

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101
Q

How much does 1 L of water weigh?

A

2.2 lbs = 1 kg

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102
Q

What is the most prevalent cation in the ICF? in the ECF?

A

ICF: potassium
ECF: sodium

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103
Q

What is isotonic, hypotonic, and hypertonic?

A

isotonic: osmolarity is the same as normal plasma, no osmosis
hypotonic: solutes are less concentrated than plasma, water moves into cells
hypertonic: solutes are more concentrated than plasma, water moves out of cells

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104
Q

What forces are responsible for fluid movement in and out of the capillaries?

A

hydrostatic pressure: force fluids in a compartment by pushing against the cell membrane or vessel wall, as the heart contracts hydrostatic pressure moves blood through vessels and as you get closer to the capillaries the pressure decreases but is still enough to move fluids

oncotic pressure is responsible for moving fluid into the tissues

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105
Q

What happens when the forces responsible for fluid movement in and out of capillaries is disrupted?

A

edema

if there’s an increase hydrostatic pressure in veins fluid cannot move into the capillary and will stay in the tissues

if there’s a decrease in oncotic pressure due to loss of plasma proteins fluid cannot enter the capillaries

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106
Q

What are the clinical manifestations of fluid volume overload?

A

bounding full pulse, distended neck veins, high bp, SOB, moist crackles

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107
Q

What are the clinical manifestations for volume deficit?

A

increased hr, constricted blood vessels, weak, thready pulse, orthostatic changes, increased RR (low perfusion rates), skin turgor tenting (in older adults loss of skin elasticity will complicate this)

108
Q

What is magnesium necessary for?

A

DNA and protein synthesis, metabolize carbohydrates, sodium/potassium pump, muscle contraction and relaxation, normal neurological function

109
Q

What is the second most abundent intracellular cation?

A

magnesium

110
Q

Where is magnesium mostly stored?

A

muscles and bones

111
Q

Which foods contain a high amount of magnesium?

A

green vegetables, nuts, peanut butter, bananas, oranges, chocolates

112
Q

How is magnesium levels regulated?

A

when levels are low GI absorption will increase and renal reabsorption will increase

113
Q

What is the normal range for magnesium?

A

1.3 to 2.1 mEq/L

114
Q

What causes hypermagnesemia?

A

increase intake of magnesium (antacids, milk of magnesia), excess IV magnesium administration (preclampsia to relax muscle contractions, reduce BP, and prevent seizures) and kidney insufficiency

115
Q

What are signs and symptoms of hypermagnesemia?

A

lethargy, facial flushing, hypotension, nausea and vomiting, weakened or delayed reflexes

116
Q

What can occur if hypermagnesemia is untreated?

A

deep tendon reflexes become more impaired, coma, respiratory depression, cardiac arrest, and then death

117
Q

How can you treat hypermagnesemia?

A

removing the source, limiting intake, fluid and diuretics for those with good kidney function (IV furosemide), dialysis for those with renal disease, calcium gluconate (for those approaching coma and cardiac arrest)

118
Q

What are the causes for hypomagnesemia?

A

GI fails to absorb magnesium due to: excessive fluid loss from GI, fasting or starvation, alcoholism (poor nutritional intake and absorption), PPIs and some diuretics, uncontrolled blood sugar

119
Q

What are signs and symptoms for hypomagnesemia?

A

muscle cramps, hyperactive reflexes, depression, anxiety, confusion, tetany, seizures, positive chvostek’s and trousseau’s sign

120
Q

How can you treat hypomagnesemia?

A

treat the cause, supplementation, increase dietary intake, IV Mg sulfate (if severe)

121
Q

What are the normal values for sodium?

A

136 to 145 mEq/L

122
Q

What is the RDA maximum for those with functioning organs?

A

2300 mg, 1 teaspoon

123
Q

What causes hypernatremia?

A

decreased water intake, excessive intake of sodium PO or IV (hypertonic tube feeding without water supplement), excessive insensible water loss (heat stroke, high fever), excessive diarrhea, diabetes insipidus (excess diuresis)

124
Q

What are the signs and symptoms of hypernatremia?

A

cellular dehydration, intense thirst, sticky mucous membranes, dry lips, flushed skin, red, rough, dry tongue, disorientation, lethargy, hallucinations

125
Q

What are some nursing interventions for hypernatremia?

A

restricting sodium, monitoring sodium content, monitor for behavioral changes (seizure percautions), excessive thirst, sufficient water is available with tube feedings

126
Q

How can you treat hypernatremia?

A

give water, IV infusions with salt free IV solution

127
Q

What is a caution with treating severe hypernatremia and hyponatremia?

A

if severe or chronic do not treat too fast to prevent swelling of cells especially in the brain

128
Q

What causes hyponatremia?

A

water intoxication, excessive loss of sodium (GI, burns, wounds), adrenal insufficiency, incorrect rehydration after profuse sweating

129
Q

What are some signs and symptoms of hyponatremia?

A

cold, clammy skin, dry mucous membranes, rapid, weak, thready pulse, orthostatic hypotension, nausea, vomiting, diarrhea, abdominal cramps indifference, confusion and irritability, feeling of doom

130
Q

How can you treat hyponatremia?

A

restrict water, give loop diuretics, isotonic solutions, if severe give small amounts of 3% NaCl

131
Q

What is potassium vital for?

A

neuromuscular, cardiac, and smooth muscle function

132
Q

What is the normal values for potassium?

A

3.5 to 5.0 mEq/L

133
Q

How is potassium primarily lost?

A

kidneys

134
Q

What foods are high in potassium?

A

bananas, spinach, vegetables

135
Q

What are the causes of hyperkalemia?

A

excessive intake, shift of K out of cells due to cell lysing (trauma, infections, crush injuries, severe burns, sepsis, acidosis), problems with elimination (renal insufficiency/failure)

136
Q

Who is most at risk for hyperkalemia?

A

very rare in those with functioning kidneys, seen in older adults especially if they are on potassium sparing diuretics, ACE inhibitors (prils), and potassium supplement

137
Q

What are signs and symptoms of hyperkalemia?

A

hyperactivity of smooth muscle, irregular, slow hr, EKG changes, lower extremity weakness, muscle twitching leading to paralysis, irritability, anxiety

138
Q

How can you treat hyperkalemia?

A

limit intake of K, increase fluids or administer diuretics (typically sufficient treatment), dialysis, kayexalate (ion exchange resin that will exchange K for Na in the intestines, takes a while to work), force K back into cells by stimulating Na/K pump with IV insulin with glucose (insulin for those who are not diabetic need to avoid hypoglycemia hence the glucose)

139
Q

What are the causes for hypokalemia?

A

diarrhea, vomiting, NG suctioning, inadequate intake (starvation, diet low in K), giving a lot of insulin for DKA

140
Q

What are the signs and symptoms of hypokalemia?

A

paresthesia (tingling, prickling, numbness, “pins and needles”), decreased reflexes, weak, thready pulse, EKG changes, muscle weakness, leg cramps, fatigue, abdominal distension, constipation, nausea and vomiting

141
Q

What are some nursing interventions for hypokalemia?

A

monitor for EKG changes, caution in patients on digoxin (for HR and Afib, could lead to toxicity), educate about abuse of laxatives and diuretics, caution with K supplements

142
Q

How can hypokalemia be treated?

A

potassium supplements (if IV: diluted and given slowly 10-20 mg/hr), increase daily intake

143
Q

What is calcium used for?

A

transmission of nerve impulses to muscles and formation of bones and teeth

144
Q

What is the normal range for calcium?

A

9 to 10.5 mg/dL

145
Q

What causes hypercalcemia?

A

hyperparathyroidism (increase in PTH will signal to the intestines and kidneys to reabsorb Ca and stimulate osteoclast activity), malignancies with and without bone involvement (secrete hormones that mimic PTH), prolonged immobility (increase osteoclast activity)

146
Q

What are signs and symptoms of hypercalcemia?

A

lethargy, weakness, decreased muscle tone, depressed reflexes, flank pain (kidney stones), cardiac arrest

147
Q

What are some nursing interventions for hypercalcemia?

A

increase mobilization, encourage oral intake, force fluids to prevent kidney stones, caution for those on digitalis

148
Q

How can you treat hypercalcemia?

A

hydration (increase excretion of calcium), loop diuretic (furosemide), synthetic calcitonin (stop osteoclast activity and inhibit calcium reabsorption by intestines and kidneys)

149
Q

What causes hypocalcemia?

A

decreased intake, poor absorption, vitamin D deficiency, kidney failure, surgical removal of part of parathyroid glands

150
Q

What are signs and symptoms of hypocalcemia?

A

muscle cramps, hyperactive relfexes, depression, anxiety, confusion, tetany, seizures, positive chvostek and trousseau sign

151
Q

How can you test for a chvostek and trousseau sign?

A

chvostek: tap cranial facial nerve which will elicit tetanus of the face

trousseau: inflate bp cuff for a few minutes which will elicit carpal spasm within three minutes

152
Q

How can you treat hypocalcemia?

A

PO or IV calcium supplement, vitamin D supplement, increase dietary intake, calcium gluconate

153
Q

What is the difference between oxygenation and ventilation?

A

oxygenation is the process of obtaining O2 from the atomspheric air and making it available to the organs and tissues of the body

ventilation involves inspiration and exhalation

154
Q

What is the normal oxygen saturation levels?

A

95 to 100%

155
Q

What is the fetal development for gas exchange?

A

4 to 17 weeks: major structures of the lung develop (larynx, trachea, bronchi, buds of the lung)

16 to 24 weeks: bronchi and terminal bronchioles enlarge, vascular structures start to develop, primitive alveoli are formed

24 weeks to term: alveoli are formed and lungs mature

35 weeks: lungs are considered to be fully developed

156
Q

What happens to fetuses stressed in utero? What can be the cause of the stress?

A

speed up their lung development by increasing cortical steroids and accelerate development of lungs; decrease in placental blood flow (causing hypoxia) due to hypertension, placental insufficiency, or infection

157
Q

What are some lifespan considerations for babies?

A

nose breathers until about three months (problem with colds and influenza), sneeze to clear the nose, irregular respiratory patterns (30 to 60 breaths per minute, brief pauses (10s) between breaths)

158
Q

What are some lifespan considerations for older adults?

A

diminished strength of respiratory muscles can lead to reduced force inhalation and exhalation (less deep of breaths and weaker cough = hard lung clearance), alveoli changes (less elastic and more fibrotic = more prone to dyspnea), respiratory infections are more serious, fewer erythrocytes

159
Q

What is asthma? Which sex is often more effected?

A

chronic inflammatory disease of the airways but after an exasperation the lungs will usually return to baseline; females are more than males

160
Q

What are some clinical manifestations of asthma?

A

wheezing, cough, SOB, dyspnea, chest tightness, persistent cough through the nigh or early in the morning,

161
Q

What is silent chest?

A

very severe asthma exasperation, significant wheezing can be heart at first and then it will stop, this indicates air not being moved at all

162
Q

What is status asthmaticus?

A

life threatening asthma exasperation that can lead to acute respiratory failure and no matter what is given the lungs do not respond and therefore the patient will need intubation

163
Q

What are the types of asthma?

A

intermittent: symptoms occur less than 2x a week, exacerbations are brief and with no interference with normal activity

mild persistent: symptoms occur more than 2x a week, exacerbations, minor activity limitation

moderate persistent: daily symptoms, daily use of inhalers, nighttime symptoms more than 1 time a week, some limitations to activity

severe persistent: continual symptoms, extremely limited physical activity, frequent nighttime symptoms

164
Q

What type of diagnostic studies can be done for asthma?

A

history and physical assessment to determine triggers and severity, pulmonary function tests, peak expiratory flow rate, chest xray (if suspect infection), allergy skin testing, blood test (ABG if suspect infection)

165
Q

What is a pulmonary function test? What does it measure? How is it performed? How are the results analyzed?

A

diagnoses pulmonary diseases, monitors the disease progression, evaluates disability, and assess response to bronchodilators; measures lung volumes and airflow; spirometer; results compared to the predicted value based on age and sex

166
Q

What is forced vital capacity? What value indicates a disorder?

A

amount of air that can be quickly and forcibly exhaled after maximum inspiration, if value is less than 80% predicted

167
Q

What is FEV1? What does it measure? What value indicates a disorder?

A

amount of air in the first second of quick and forced exhalation after maximum inspiration; grade of severity of obstruction; less than 80% of predicted

168
Q

What is peak expiratory flow rate?

A

rate during forced exhalation

169
Q

What are some types of pharmaceutical treatments for asthma?

A

SABA, LABA, inhaled corticosteroids, anti-inflammatories, combination, leukotriene modifiers, anticholinergics

170
Q

What is albuterol? Onset of action?

A

short acting B2 adrenergic agonist that will cause bronchodilation; works within minutes

171
Q

What is salmeterol? Onset of action?

A

long acting B2 adrenergic agonist that will cause bronchodilation; works in about 30 to 45 minutes

172
Q

What is fluticosone? Onset of action?

A

inhaled corticosteroid that will have long term control to reduce local inflammation, prescribed daily or seasonally; takes about 1 to 2 weeks for maximum effectiveness

173
Q

What is prednisone?

A

systemic anti-inflammatory that will have quick improvements during an asthma exacerbation

174
Q

What is the difference between steroids and inhaled corticosteroids?

A

steroids will have a quicker onset of action and a systemic effect compared to inhaled corticosteroids which works locally and takes 1 to 2 weeks for maximum effectiveness

175
Q

What are some examples of a combination medication for asthma? Who is it typically prescribed for? MOA?

A

fluticasone/salmeterol and budesonide/formoterol; for those who are not well controlled on SABA and inhaled corticosteroids; the LABA will open up the airways and the corticosteroid will reduce inflammation

176
Q

What is montelukast? MOA? Usage?

A

leukotriene modifier that will prevent the binding of leukotrienes at its receptor; reduce the inflammatory response of an asthmatic exasperation; asthma maintenance and allergic rhinitis

177
Q

What is ipratropium? MOA? Usage?

A

short acting anticholinergic; prevents bronchospasms by relaxing smooth muscle around the bronchi; severe asthmatic exacerbations, COPD (reduce secretions)

178
Q

What is the difference between anticholinergics and SABA for asthma?

A

SABA will work in the small airways while anticholinergics cannot

179
Q

What are the causes of COPD?

A

smoking (primary risk factor), occupational chemicals and dust, air pollution, asthma

180
Q

Which sex is most effected by COPD?

A

affects men and women almost equally due to increased tobacco usage among women in high income countries

181
Q

How can you cure COPD?

A

it is un-curable, it is a slow progressive disease but its progression can be slowed with treatment

182
Q

What is the pathophysiology of COPD?

A

noxious particles and gasses will cause: inflammation of central airways (increase mucus production and narrowing of airways), remodeling of alveoli (bullae and bleb formation), parenchymal destruction, and permanent pulmonary vascular changes (destruction/dysfunction of cilli decreasing airway clearance)

183
Q

What is the most defining characteristic of COPD? Cause?

A

chronic air trapping; inability to expire all air

184
Q

What are bullae and blebs?

A

big air spaces in the lung parenchyma created with airway remodeling due to COPD that will reduce effective gas exchange due to lack of vasculature

185
Q

What are the clinical manifestations of COPD?

A

chronic cough, sputum production, dyspnea upon exertion, wheezing, chest tightness, weight loss/anorexia, anterior-posterior diameter of the chest is increased, general fatigue, tripod position-sitting, purse lips on expiration, hypoxemia, polycythemia, cyanosis, clubbing of digits

186
Q

Which clinical manifestation could make it harder for someone to realize they may have COPD? Why?

A

chronic cough could be dismissed as being due to smoking or age-related changes

187
Q

Why does a barrel chest occur with those with COPD?

A

chronic overinflation of lungs cause the rib cage to stay partially expanded

188
Q

Why does purse lips expiration occur in those with COPD?

A

helps to prolong exhalation and prevent collapsing of alveoli and air trapping and allowing as much air to exit as possible

189
Q

Why does polycythemia occur with COPD? What are the dangers?

A

an increase in RBC production is done to compensate for poor gas exchange; leads to an increase in blood viscosity and an increased risk for strokes and clots

190
Q

What diagnostic studies can be done for COPD?

A

pulmonary function test (FEV1 and FVC ratio is less than 0.7), ABGs

191
Q

What are the classifications of COPD severity?

A

Gold 1: mild, FEV1 is greater or equal to 80% predicted

Gold 2: moderate, FEV1 is 50 to 60% predicted

Gold 3: severe, FEV1 is 30 to 50% predicted

Gold 4: very severe, FEV1 is less than 30% predicted

192
Q

What are some non-pharmaceutical treatments COPD?

A

influenza and pneumococcal vaccinations, smoking cessation (single most effective and cost-effective intervention), nutrition (small meals, rest at least 30 min before eating, bronchodilators before eating), relieve symptoms and improve exercise tolerance

193
Q

What are some pharmaceutical treatments for COPD? When are they used?

A

when FEV1 is between 60 and 80 of what is predicted bronchodilators can be used

when FEV1 goes below 60 and person is symptomatic an anticholinergic or LABA may be prescribed (ipatropium bromide and salmeterol)

194
Q

What are the chances two carriers of the CF gene have a child with CF? Have a child with a CF gene?

A

25%
50%

195
Q

Which organs are most effected by CF?

A

pancreas and lungs

196
Q

What is the pathophysiology of CF?

A

the CF gene inactivates the CFTR protein (a protein responsible for regulating sodium and chloride movement in and out of cells), causing a blockage of the sodium chloride channel and causing an increase in thick and sticky mucus secretions that will attach to the surface of the airways, GI tracts, and sweat glands

197
Q

What happens to the lungs during CF?

A

increase viscosity of mucous leads to poor ciliary action (stuck together by mucus) leads to retained mucus, bacterial growth in alveoli is easier leading to more frequent infections (p. aeruginosa, S. aureus, H. flu, E. coli, klebisella), progressive lung fibrosis and dysfunction

198
Q

What happens to the GI system with CF?

A

thick mucus block of pancreatic duct preventing enzymes from reaching the duodenum leading to impaired digestion of fats and proteins and scarring of the pancreas

characteristics of type 1 and 2 diabetes: under developed islet cells in utero and destruction of cells, islet cells make insulin but not enough developed islet cells are present and the destruction of the functioning islet cells is occuring

liver biliary obstruction and fibrosis

199
Q

What are the clinical manifestations of CF?

A

variable, steatorrhea (bulky, frothy stool with proteins due to their indigestion, most common: failure to thrive, impaired digesting, constant respiratory infections

200
Q

What are the in utero manifestations of children with CF?

A

meconium ileus, a small intestinal blockage with thick puddy meconium

201
Q

What is the gold standard for a diagnosis of CF?

A

sweat chloride test, a small electrical current is placed to stimulate sweating, the sweat is collected and sodium chloride concentration is analyzed, if there’s more than 60 mmole/L it is positive, CF patients have 4 times the normal amount of sodium chloride in their sweat due to not being absorbed in sweat ducts

202
Q

What is immunoreactive trypsinogen?

A

standard newborn screening for CF, high levels of IRT suggest possible CF and will require further testing as it is not diagnostic

203
Q

What is a diagnosis of CF based on?

A

Hx of disease in family, absence of pancreatic enzymes, positive sweat chloride test

204
Q

What are the treatment goals for CF?

A

minimize pulmonary infections, improving aeration with bronchodilators and chest physiotherapy, removal of thick secretions (via pulmozyme), aggressive use of antimicrobials

205
Q

What is pulmozyme?

A

medication for CF that will aid in reducing viscosity of mucus secretions

206
Q

What nutritional changes should CF patients follow?

A

ensuring a high protein and high caloric diet (may need G tube placement for supplementation), replacing pancreatic enzymes before every meal and snack (lipase, protease, amylase), fat-soluble vitamin supplementation (ADEK)

207
Q

What are some complications that adult CF patients can experience?

A

CF related diabetes, osteoporosis (due to malnutriton and malabsorption), liver problems (cirrhosis), female have difficulty conceiving but usually can do so while males cannot conceive due to blockage or absence of vas deference, increasing lung disease that may need transplantation

208
Q

What are some risk factors for pneumonia?

A

greater than 65 years of age, air pollution, prolonged immobility, debilitation illness, immunosuppressed/compromised, smoking, intubation

209
Q

What are the classifications of pneumonia? Their common causes?

A

community acquired: person has not been hospitalized or in a LTC within 14 days after onset of symptoms, common causes: strep. pneumoniae, H. influenza, fungi, viruses

hospital acquired (nosocomial): occurs 48 hours after hospital admission or 48 hours or longer after intubation, common cause are gram negative bacilli (psudomonas aeruinosa, E. coli) and staph. aureus

aspiration pneumonia: entrance of foreign materials into bronchial tree

opportunistic pneumonia: weakened immune system allows normally harmless organisms can flourish and grow out of control, typically caused by fugal including: pneumocytis jiroveci, cytomegalovirus, myobacterium avium

necrotizing pneumonia: rare complication of bacterial lung infection that causes the lung tissue to turn into thick liquid mass

210
Q

What is empiric antibiotic theory?

A

therapy directed at the most likely cause of the disease, treat early because do not want to wait for cultures as the disease could get worse

211
Q

What is the risk of hospital acquired pnuemonia?

A

mortality rate of up to 33%, worried about antibiotic resistant bacteria

212
Q

Who is most at risk of aspiration pneumonia? What are the clinical manifestations?

A

intubated patients, LOC due to: stroke (dysphagia), head trauma, seizures, alcohol intoxication; frothy sputum, cough, wheezing, decreased O2

213
Q

Who is most at risk for opportunistic pneumonia?

A

immunocompromised, those with AIDS or receiving chemotherapy, bone marrow suppression/transplants, or organ transplant

214
Q

How can you treat necrotizing pneumonia?

A

long term antibiotics and surgery

215
Q

What is the pathophysiology of pneumonia?

A

a foreign agent enters the lungs and release endotoxins causing an increased production of mucus, consolidation of alveoli (they fill with fluid and debris) which lowers gas exchange

216
Q

What are the clinical manifestations of pneumonia?

A

cough (may or may not be productive), fever, chills, dyspnea, tachypnea, sharp or burning pain in chest when breathing or coughing, older adults first present with new onset confusion

217
Q

What are the diagnostic tests for pneumonia?

A

chest radiography, complete blood count (see a shift to left), sputum culture (what’s growing) and sensitivity (what kills it), gram stain, blood gases or pulse ox

218
Q

What are some nursing considerations for those with pneumonia?

A

HOB greater than 30 to allow for easier ventilation and prevent aspiration, good orgal care, reposition every two hours

219
Q

What type of pharmaceutical treatments are there for pneumonia?

A

antibiotics after gram stain, bronchodilators for inflammation, guafensin for thinning mucus (need to increase fluid intake)

220
Q

What is guafensin? Nursing consideration?

A

thin/break up mucus for pneumonia; increase fluid intake

221
Q

What type of vaccinations are available for pneumonia? Who gets them?

A

Prevnar 13: children less than 5
Pneumovax 23: for adults older than 65

222
Q

Who is at risk for pneumonia?

A

chronic illnesses, recovering from severe illness, in LTC, adults with asthma or who smoke

223
Q

When would you give IV KCl? What are some considerations when giving KCl?

A

hypokalemia; needs to be diluted and given at 10 mEq/hr, invert IV bag several times to ensure even distribution, do not add to a hanging IV bad to prevent bolus dosage, assess for phlebitis, infiltration, and digitoxin toxicity

224
Q

What is the stepwise treatment plan for those with intermittent asthma?

A

maintain current step, regular follow up every 1 to 6 months to maintain control and consider step down if well controlled for at least 3 months

225
Q

What is the stepwise treatment plan for those with mild persistent asthma?

A

step up one step, reevaluate in 2 to 6 weeks, for side effects consider alternative treatment options

226
Q

What is the stepwise treatment plan for those with moderate and severe persistent asthma?

A

consider oral corticosteroids, step up 1 or 2 steps and reevaluate in 2 weeks, for side effects consider alternative treatment options

227
Q

What are physiological differences for infants and elimination?

A

lower GFR, limited tubular reabsorption and excretion can cause cloudy urine that should become more concentrated within three months

228
Q

What are the voiding patterns for infants?

A

first void is within 48 hrs of birth
will begin with 2 to 6 times a day and will increase to 6 to 8 within the first four days of birth

229
Q

What are the elimination considerations for preschoolers?

A

most develop urinary control between 2 to 5 years, require instruction on wiping

230
Q

What are elimination considerations for school-age children?

A

more regular voiding patterns, enuresis is common, noctural enuresis (girls will typically develop mature sleep cycle before boys)

231
Q

What are the elimination considerations for pregnancy?

A

increased GFR by 50% in the first trimester and continues to increase throughout pregnancy (due to hormones), increased urinary frequency (during second trimester symptoms can decrease but during third trimester frequency will increase), glycosuria (impaired tubular reabosorption of glucose)

232
Q

What are elimination considerations for older adults?

A

decline in renal function, decrease in autonomic regulation, decerease in renal blood flow due to atrophy, more concentrated urine, decrease in specific gravity, more fluid and electrolytes excreted at night, excretion of medications is impaired increasing the risk of overdose

233
Q

What diagnostic labs are done to view elimination?

A

urinalysis through sterile or clean catch, 24 hr collection for creatinine clearance to approx GFR, BUN, creatinine (most reliable blood test for renal function), sodium potassium

234
Q

Which radiology tests can be done to view elimination?

A

KUB for kidney stones, angiogram for renal blood supply, ultrasound for massess and obstructions, cytoscopy to view interior bladder, remove kidney stones, and biopsy lesions, uroflometry (urine volume and speed in a single void to view bladder or sphincter dysfunction), kidney biopsy

235
Q

What are some genetic considerations and non-modifiable risk factors?

A

women have an increased risk for incontinence, men at increased risk for retention (gets worse due to BPH or prostate cancer), disability and family hx

236
Q

What are some modifiable risks for altered urination?

A

pregnancy, obesity, UTI, consumption of bladder irritants, smoking

237
Q

What are bowel elimination considerations for newborns and infants?

A

meconium occurs within 24-48 hours,, warn parents as to what it will look like

transitional occurs at day 3 of feeding, thin and less sticky than meconium

milk stool occurs at day 4 of feeding, if breastfed: mustard and cottage cheese with a sour milk odor. if formula fed: pale yellow to light brown, firmer, slightly more odor than breastfed

238
Q

What are bowel elimination considerations for toddlers?

A

daytime control occurs typically 2.5 years of age, usually accomplish bowel training before bladder

239
Q

What are bowel elimination considerations for school age children and adolescents?

A

bowel habits are similar to adults, patterns vary

240
Q

What are bowel elimination considerations for pregnancy?

A

delayed gastric emptying, decreased peristalsis, bloating and constipation (increased absorption of water from colon), hemorrhoids (after birth stool softeners need to be ordered)

241
Q

What are bowel elimination considerations for older alduts?

A

constipation is common due to slower peristalsis, reduced activity levels, inadequate fluid and/or fiber, medications, dimminished sensory perception

incomplete emptying

242
Q

What are diagnostic labs done for bowel elimination?

A

H&H for occult bleeding, fecal analysis

243
Q

What diagnostic tests are done for bowel elimination?

A

x-ray imagining via barium enema

colonoscopy for direct visualization

244
Q

What are some genetic considerations and non-modifiable risk factors for bowel elimination alterations?

A

young children and older adults at high risk for diarrhea, constipation, fecal incontinence

women are high risk for fecal incontinence especially after pregnancy

245
Q

Where can elimination alterations occur? Why? Causes?

A

prerenal: decreased blood flow to kidneys, HF, dehydration, hemorrhage

renal: injury to glomeruli or tubules, diabetes, transfusions, injury

postrenal: acute obstruction effect the normal flow of urine out of both kidneys, enlarged prostate or bladder/kidney stone, tubule obstruction or renal injury

246
Q

What is oliguira?

A

decreased urine production, can be associated with impending renal failure

247
Q

What are the causes for urinary incontinence?

A

DRIP
Delirium, dehydration, depression
Restricted mobility, rectal impaction
Infection, inflammation, impaction
Polyuria, polypharmacy

248
Q

What are the types of urinary incontinence?

A

stress: sudden increase in intrabdominal pressure (during laughing, coughing, sneezing) due to relaxed pelvic floor musculature, atrophy of female urethra from decreased estrogen, prostate surgery for BPH or prostate cancer

urge: uncontrolled contraction or overactivity of detrusor muscle due to overactive bladder, alzheimer’s, and parkinson’s

overflow: pressure of urine is overfull bladder and overcomes sphincter causing small amounts of leakage throughout the day due to bladder or urethral outlet obstruction, neurogenic bladder

reflex: involuntary voiding without warning or stress due to spinal cord lesion or injury

post-traumatic or surgical: vesicovaginal or urethrovaginal fistula allowing passage of urine through the vagina due to injury

functional: loss of urine from cognitive, functional, or environmental factors, due to affecting balance and mobility

249
Q

What is oxybutynin?

A

anticholinergic used a lot with urge incontinence to calm the bladder and reduce frequency

250
Q

What is tamsulosin?

A

alpha adrenergic blocker for overflow incontinence to help with urethral sphincter resistance to urinary overflow

251
Q

Which medications can help with reflex incontinence?

A

diazepam or baclofen

252
Q

What can vaginal estrogen cream be used for?

A

stress and urge incontinence to reduce thinning of vaginal tissues and thereby strengthening the tissues

253
Q

What can cause urinary retention?

A

bladder outlet obstruction such BPH, deficient detrusor contraction (due to neurologic disease affecting the sacrum, diabetes, overdistension, chronic alcoholism, drugs)

254
Q

What is the pathophysiology of fecal incontinence?

A

impaired motor function, impaired sensory function, fecal impaction (liquid stool will leak around the fecal impaction)

255
Q

What can cause fecal incontinence?

A

manifestation of another disorder: neurological disorders (stroke, dementia), traumatic injuries (surgical, complications from childbirth), inflammatory process (IBS)

256
Q

What are some nursing interventions for fecal incontinence?

A

bowel assessment, bowel training (digital stimulation or tap water enemas for neurogenic bowels (spinal cord injuries)), maintain perineal skin integrity

257
Q

What is ammodium?

A

slows down GI and allows for more water absorption during diarrhea

258
Q

What is solesta?

A

injection into the anal canal to help build up tissues to help with better closure of the muscles during fecal incontinence

259
Q

What is biofeedback?

A

helps coordinate sphincters and strengthening of contractions for fecal incontinence, must have sensory and motor nerves

260
Q

What is encorpresis? Cause? Who is most at risk? Treatment?

A

abnormal elimination pattern leading to recurrent fecal incontinence by a child who should have achieved bowel continence; chronic constipation causes child to associate defecation with pain so they continually hold their stool causing a large accumulation to then stretch out the colon; children, predominantly boys; fecal impaction needs to be removed with stool softeners and laxatives, then need to dissociate pain with defecation, then train how to have regular bowel movements without pharmaceuticals

261
Q

What can cause acute constipation? Chronic constipation?

A

dehydration, medications, immobility; opioid usage, laxative abuse (dilate colon, reduce muscle tone), obstruction

262
Q

What is methylcellulose? MOA? Nursing considerations?

A

bulk forming laxative; high in fiber, absorbs water to increase bulk; increase water intake

263
Q

What is magnesium hydroxide and magnesium citrate? MOA?

A

saline laxative, increases osmotic pressure within GI, causing more water to enter intestines

264
Q

What is polyethylene glycol, sorbitol, glycerin, and lactulose?

A

hyperosmotic laxative that increases water inside GI

265
Q

What is senokot

A

stimulant laxative that increases peristalsis via intestinal nerve stimulation

266
Q

What are the types of starvation?

A

starvation related (nutritional needs not met, usually chronic, no inflammation is typically involved)

chronic disease related (disease processes effecting nutritional status, milk to moderate inflammation present),

acute disease or injury related (marked, high, inflammatory response due to significant burns and trauma and spesis)

267
Q

What are some common examples of potassium sparing diuretics?

A

amiloride, spironolactone, triamterene, eplerenone

Health and Illness (4 decks)

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