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33 Cards in this Set
- Front
- Back
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What is COPD |
- slowlyprogressive disease that is characterized by a gradual loss of lung function - includes chronic bronchitis and emphysema |
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What is emphysema? |
- Abnormal – permanent enlargement ofalveoli |
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etiology of emphysema |
- Can often happen as a result of chronic bronchitis - alpha 1 anti-tryspin (helps defend against toxins) deficiency; Inherited disorder that causes significant reduction in the naturally occurring protein AAT - Inflammationor enzymes destroy lung tissue with increases loss of surface area and decreases amount of surfactant
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pathophys of emphysema |
- loss of connective tissue, airway collapse during exhale; bronchioles lose elasticity and trap air in lungs - Cigarette smoke; increases free radicals; increases damage to cell membranes - Chronic presence of inflammatory cells releases elastase which causes destruction of elastin - Decreases recoil in the alveoliwhich is needed to force air out of the lungs - alveoli can rupture putting air into pleural space, pressure is disrupted and lung can collapse |
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signs and symptoms of emphysema |
- barrel chest due to trapped air - decreased air flow (FEV) - inspiration not impaired, but more difficult to exhale (pursed lips to push out air); Use of accessory muscles forexhalation - Hypercapnia, respiratory acidosis - Hypoxemia only in last stages(due to exhaustion) - Dyspnea, orthopnea |
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What is chronic bronchitis? |
- chronic inflammation of the airways |
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etiology of chronic bronchitis |
- Repeated exposure of airways topollutants leads to inflammatory response which causes increased sputum production andcough - Cigarette smoking = decrease cilia function, phagocytosis, IgA deficiency (increases susceptibility to infection) |
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pathophys of chronic bronchitis |
- Chronic inflammation causeshyperplasia of mucous cells: airway edema and mucus production - Cilia become damaged and then areunable to help clean mucus from the airways - Walls of the airway thicken andmucous glands undergo hyperplasia - Increased airway resistance due to less space for air to travel and increased mucus - Unable to increase work ofbreathing enough to overcome hypoxemia, hypercapnia |
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signs and symptoms of chronic bronchitis |
- Decreased air flow rates ( decreased FEV) - Respiratory acidosis (too much CO2 breathed in, not enough O2 out) - Dyspnea - Signs of chronic hypoxemia(cyanosis, clubbing, secondary polycythemia) - Cor Pulmonale (alteration in right vent of heart, can cause pulmonary HTN) |
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Meds used for COPD |
- Bronchodilators to relax bronchioles and relieve shortness of breath - steroids/corticosteroids used to reduce inflammation - antibiotics - luekotriene inhibitors for inflammation - mucolytics - immune system modifier (inhibts binding of IgE and allergic response) |
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medical treatment of COPD |
- smoking cessation - oxygen therapy - vent support - lung volume reduction surgery - Lung transplant |
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nutritional issues with COPD |
- lack of intake due to shortness of breath causes weight loss - meds can cause ulcers and N/V - increased energy expenditure due to increased work of breathing - catabolism of LBM; increased breakdown, decreased intake - CO2 retention; acidosis |
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Risk of malnutrition with COPD |
- Use BMI and % weight change asprimary markers for risk |
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nutrition therapy for COPD |
- EER: 125-150% of recommended - Probably use harrisbenedict equation with stress factor or 30-35kcal/kg; pennstate on vent - protein: 1.2-1.7g - indirect calorimetry best way to judge EER if available - increase nutrient density - small frequent meals using oxygenation - no need to restrict milk - physical activity/pulmonary rehab recommended |
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supplements for COPD |
- antioxidants (reduce free radicals/damage) - omega 3s (reduce inflammation) - oral supps to increase intake |
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what is cystic fibrosis? |
- Autosomalrecessive disorder, caused by gene defect on chromosome 7 - Defective CFTR affects chloride channels of specificcells, causing imbalance of sodium/chloride exchange which causes thick,sticky mucus to clog tissue of certain organs, especially lung and pancreatictissue. - risk is 1 in 4 of developing CF |
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Effects of cystic fibrosis on lungs and pancreas |
-in lungs: thick mucus promotes the growth ofbacteria, leading to pulmonary infections, decreased lung function, andeventual mortality - in pancreas: linhibitsproduction of digestive enzymes |
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nutritional goals/markers for CF |
- Children should be greater than 50% on growth charts - men BMI greater than 23 - Women BMI greater than 22 |
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pancreatic insufficiency with CF |
- leads to fat malabsorption; not getting essential FA - use enzyme replacement therapy - goal for enzymes = 1500-2500 - enterically coated so they can make it through stomach acid and be used in intestines |
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vit and mineral supps for CF |
- ADEK required daily - Fat soluble vitamins provided inwater-miscible form - The preparations also containother, water-soluble vitamins and zinc - May also need iron and calcium - Vitamin D supplement recommendedduring winter - salt supplemented in infants |
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nutrition recs for CF |
- EER 130-150% of RDA for age - Increased energy expenditure due towork of breathing and energy losses related to malabsorption - high cal high protein - oral supplements - CF pts cannot be around each other because they can pass infections to each other more easily |
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medical treatment of CF |
- Patients are often admitted to hospitalif pulmonary function is diminished. Occasionally need a “clean-out” with IV antibiotic treatment - antibiotics - resp treatments - bronchoscopies - sinus surgery |
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At home treatments for CF |
- vest therapy; shakes and removes mucus - huff cough - enzymes with every meal - snacks and supps - lots of meds - PPI's (decrease acid in GI) inhaler (bronchodilator), enzymes, vitamins; hard for people to follow - must avoid smoke and practice good hygiene |
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Comorbidities of CF |
- GERD - Diabetes - osteoporosis - liver disease - hearing loss - sinusitis - end stage lung disease -> transplant |
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monitoring in CF |
- height/length - stool pattern/enzyme dosage - monitor serum vitamin levels/vitamin and mineral dosage - diet history - DEXA scan - glucose intolerance testing |
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what is BPD |
- bronchopulmonary dysplasia - Chronic lungdisease that affects primarily pre-term infants, due to immature lung tissue,inflammation, and inadequate oxygenation |
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etiology of BPD |
- Premature birth (low gestational age) - Inflammationof lung tissue - Surfactantdeficiency - Geneticpredisposition - Patent ductus arteriosus - Infection |
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pathophys of BPD |
- Inadequatelung function and gas exchange by the alveoli due to weak and fragile underdeveloped tissues - Requiringartificial oxygen supplementation at highpressure, which further damages the weak lung tissue |
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medical treatment of BPD |
- time - supplemental oxygen |
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nutrition concerns for BPD |
- Lack ofEvidence-Based Nutrition Guidelines - Preterm InfantGuidelines often used - Chronicdisease – how do weprovide MNT for older patients? |
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meds for BPD |
- bronchodilators - diuretics - vasodilators - Oral andInhaled Corticosteroids |
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Nutrition rec for BPD |
- High cal 110-130kcal/kg (RDA is 100kcal) - oxygen supps effects energy needs - requirements decrease as they age - pro: 3.5-4.5g/kg/day needed for growth, increased lung function - fluids restricted to <120 ml/day to reduce edema - |
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MNT for BPD |
- usually enterally fed (poor suck/swallow reflex) - concentrated preterm infant formula if given PO ; 22- 30 kcal/oz - liquid protein if needed - multivitamin can be with or without iron - important to monitor tolerance to formula; vomiting, diarrhea, abdominal distension etc |
