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Description
Flashcards by Kristi Breese, updated more than 1 year ago
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Created by Kristi Breese
about 7 years ago
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| Question | Answer |
| -Preventable -Treatable -Chronic air flow limitation that is fully reversible -Progressive -Inflammatory response to noxious particles, usually smoking | COPD |
| COPD is the _____ leading cause of death in the US | 3rd |
| More than _____% die within 10 years of a COPD diagnosis | 50 |
| COPD is characterized by __________, ____________, and _____________. | Airflow limitation, breathlessness, exacerbations |
| COPD includes: | Emphysema Chronic Bronchitis |
| 1. Abnormal permanent enlargement of the air space distal to the terminal bronchioles. 2. Destruction of bronchioles without obvious fibrosis 3. Only 10% of patients have the pure form of this | Emphysema |
| 1. Presence of chronic productive cough for 3 or more months in each of 2 consecutive years. 2. Other cause of chronic cough must be excluded | Chronic bronchitis |
| COPD risk factors | 1. Cigarette smoking 2. Air pollution 3. Chronic infection 4. Heredity (AAT deficiency) 5. Aging 6. Occupational chemicals and dust |
| Smoking cessation can both __________ and _________ progression of COPD | Prevent and slow |
| Occupation and environmental factors have a _______ risk compared to smoking | Small |
| COPD can develop with intense or prolonged exposure to: | 1. Dusts, vapors, irritants, or fumes 2. High levels of air pollution 3. Fumes from indoor heating or cooking with fossil fuels |
| Severe, recurring __________ in childhood (and adulthood) have been associated with decreased lung function and increased respiratory symptoms in adulthood | Infections |
| The genetic risk factor for COPD | α-Antitrypsin (AAT) deficiency |
| AAT ___________ lysis of the lung tissue | Inhibits |
| Aging | 1. Some degree of emphysema is common due to physiological changes of aging lung tissue, even in a non smoker 2. Gradual loss of elastic recoil 3. Thoracic cage changes & lungs become rounded and smaller 4. Decreased total # of alveoli & loss of alveolar supporting structures. |
| Inflammation | 1. Complex, but primary process of COPD 2. Inhaled noxious particles→release of inflammatory mediators→causes damage to lung tissue→excess mucus→ongoing injury and repair→structural remodeling occurs→increased scar tissue→resulting fibrosis |
| COPD early interventions | 1. Oral medications 2. Inhaled medications |
| Oral and inhaled medications are used for patients with stable COPD to __________, ___________, & _____________. | 1. Reduce dyspnea 2. Improve exercise 3. Prevent complications |
| Most of the maintenance medications used in COPD treatment are directed at: | The potentially reversible mechanisms of airflow limitation |
| Onset of clinical manifestations | 1. Develops slowly, usually age 40-50ish 2. and usually with 20 pack-years of smoking |
| Diagnosis of COPD is considered with | 1. Cough 2. Sputum production 3. Dyspnea 4. Exposure to risk factors |
| The earliest sx of COPD is | Intermittent cough, usually in the AM |
| Patient will usually seek medical attention when | Dyspnea occurs or with infection |
| Clinical manifestions | 1. Barrel-chested 2. Characteristically underweight with adequate caloric intake 3. Chronic fatigue 4. Prolonged expiratory phases, wheezes, decreased breath sounds 5. Bluish-red color of skin (polycythemia and cyanosis) |
| Polycythemia | An abnormal condition with excessive levels of red blood cells |
| Cyanosis | Bluish discoloration of skin and mucous membranes |
| COPD Exacerbations | 1. Signaled by change/worsening; different than daily patterns 2. Increases in: dyspnea, cough, sputum 3. Flare ups require changes in management 4. The more severe the COPD, the poorer the outcomes of exacerbations |
| Depression may be _______ times more likely for COPD patients | Four |
| Anxiety complications | 1. Respiratory compromise 2. Dyspnea 3. Hyperventilation |
| Diagnosis of COPD is confirmed by | Pulmonary function tests |
| True or False: 1. H & P is important in the diagnostic workup 2. The chest x-ray is not a very good indicator of the severity of disease early on. It may show hyperinflation but this is only one piece of the puzzle | TRUE |
| The most significant findings of pulmonary functions tests are | The increased resistance to expiratory airflow |
| 10 signs of COPD exacerbation (first 5 on this flashcard) | 1. Shortness of breath 2. Noisy breathing 3. Worry (anxiety) 4. Irregular (uneven) breathing 5. Cough |
| 10 signs of COPD exacerbation (last 5 on this flashcard) | 6. Changes in skin or nail color 7. Trouble sleeping or eating 8. Can't talk 9. Early morning headache 10. Swollen ankles or belly pain |
| Indications for ICU admit | 1. Severe dyspnea that responds inadequately to emergency treatment 2. Confusion, lethargy, coma 3. Persistence of: worsening hypoxemia, increasing hypercapnia, severe or worsening respiratory acidosis |
| Other COPD diagnostic studies | CBC, electrolytes, coagulation studies, troponins, inflammatory markers, blood culture, ABGs, AAT levels, 12 lead ECG, CXR, Spiral CT |
| Typical ABG findings in exacerbations | 1. Low PaO2 and saturations 2. Increased PaCO2 3. Normal or decreased pH as exacerbation progresses 4. Increased bicarbonate level found in late stages or exacerbations of COPD |
| What is good to look at on a CBC? | 1. H&H (higher in COPD patient) 2. WBC (infection?) |
| How do we care for a COPD patient? | 1. Assess, assess, assess 2. Establish severity 3. Positioning (tripod, elevate HOB) 4. Administer meds, focus on inhaled if possible 5. Diagnostics 6. Long term care goals 7. End-of-life planning |
| Acute airway management in a COPD patient | 1. Oxygen therapy 2. First things first... AD? DPA? 3. Underlying issue - can this be fixed? Can patient return to baseline? 4. CPAP/BiPAP 5. Endotracheal intubation (nasal v. oral) 6. Tracheostomy |
| COPD Drug Therapy | 1. Bronchodilators 2. Inhaled corticosteroid therapy 3. Oxygen 4. Oral corticosteroids - usually prednisone 5. Methylxanthines (theophylline) 6. Mucolytics 7. Beta blockers 8. Antibiotics |
| Bronchodilators | 1. Relaxes smooth muscle in the airway 2. Improves ventilation of the lungs 3. Inhaled route is preferred 4. Both beta agonists & anticholinergics 5. Both short acting & long acting |
| Inhaled corticosteroid therapy | Used for moderate to severe cases |
| Antibiotics in COPD care | 1. Oral - 2nd & 3rd generation cephalosporin, macrolides, doxycycline, flouroquinolone 2. IV - same as oral AND beta lactam antibiotic + beta lactamase inhibitor |
| COPD Collaborative Care | 1. Smoking cessation 2. Oxygen therapy 3. Respiratory & physical therapy 4. Effective coughing |
| Oxygen therapy | 1. Oxygen is considered a drug 2. Medicare will cover if Pt's O2 saturation is less than 88% 3. Goals are to reduce the work of breathing, decrease the workload of the heart, keeping sats above 90% 4. Can have low flow O2 or high flow O2 depending on Pt's needs |
| Respiratory and Physical therapy | Breathing retraining - pursed lip to prolong exhalation and diaphragmatic breathing to focus on using the diaphragm to achieve max inhalation instead of accessory muscles |
| Main goals of effective coughing | 1. Conserve energy 2. Reduce fatigue 3. Facilitate removal of secretions |
| COPD Health Promotion | 1. Vaccinate (Pneumonia & Flu) 2. Adequate rest 3. Avoid exposure to viral URI 4. Pulmonary rehab 5. Nutrition & hydration to support metabolic needs |
| COPD Nursing Diagnoses | 1. Ineffective airway clearance 2. Impaired gas exchange 3. Imbalanced nutrition: less than body requirements 4. Risk for infection 5. Insomnia 6. Anxiety and/or depression 7. Others: Self-esteem, dependence |
| Elevated pulmonary artery (PA) pressure from an increase in resistance to blood flow through the PA (usually low resistance, low pressure) | Pulmonary Hypertension |
| Common manifestations of pulmonary hypertension | 1. Dyspnea 2. Exertion & fatigue |
| Pulmonary hypertension | 1. Can be primary (idiopathic) or a secondary complication 2. Incurable |
| #1 Cause of secondary pulmonary HTN | COPD |
| Other causes of secondary pulmonary HTN | 1. PE 2. Obstructive sleep apnea 3. Autoimmune diseases; RA, scleroderma 4. Medications 5. Heart valve disease 6. Congenital heart 7. Left heart failure |
| Definitive test to diagnose pulmonary HTN | Right sided heart catheterization |
| In pulmonary HTN, dyspnea on exertion (DOE) is related to | Inability of cardiac output to increase in response to oxygen demand |
| Pulmonary HTN ________ workload of right ventricle and causes right ventricle ________ and can lead to ___________ | 1. increases 2. hypertrophy 3. cor pulmonale |
| Clinical manifestations of pulmonary HTN | 1. Dyspnea, fatigue, lethargy, chest pain 2. Increased pulmonic heart sound 3. RV hypertrophy on ECG 4. If leading to cor pulmonale will also see: peripheral edema, JVD, enlarged liver & spleen 5. Polycythemia |
| Enlargement of the right ventricle secondary to diseases of the lung, thorax, or pulmonary circulation. | Cor pulmonale |
| Causes of cor pulmonale | 1. COPD (most common) 2. Pulmonary HTN 3. Cardiac failure |
| Cor pulmonale clinical manifestations | 1. Dyspnea 2. Chronic productive cough 3. Wheezing 4. Retro/substernal pain 4. Fatigue 5. Potential for chronic hypoxemia → Polycythemia, Increased total blood volume & viscosity |
| Cor pulmonale clinical manifestations with right heart failure | 1. Peripheral edema 3+ 2. Weight gain 3. JVD 4. Full, bounding pulse 5. Enlarged liver |
| Cor pulmonale plan of care | 1. Treat underlying pulmonary problem 2. Long term O2 therapy 3. Monitor fluid, electrolyte & acid-base imbalance 4. End-stage surgical procedures include atrial septostomy (palliative) and lung transplantation |
| Goal of pharm management of pulmonary HTN and cor pulmonale | Promote vasodilation of pulmonary vasculature, reduce right ventricle overload, and reverse remodeling |
| Pharm management of pulmonary HTN and cor pulmonale | 1. CCBs - high doses, not in right sided heart failure 2. Phosphodiesterase enzyme inhibitors - given orally, contraindicated if on NGT 3. Vasodilators - both parenteral and inhaled, not for hypotensive patient 4. Endothelial receptor antagonists - oral, binds to endothelin-1 receptors with a decrease in PA pressures and increase in cardiac index |
| Pharm management of pulmonary HTN and cor pulmonale (continued) | 5. Oxygen - hypoxia is potent vasoconstrictor. Goal is to maintain sats over 90% 6. Diuretics - to manage peripheral edema 7. Anticoagulants - sx r/t thrombus 8. Inotropic agents - digoxin & sometimes theophylline |
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