Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
118 Cards in this Set
- Front
- Back
|
Define Obstructive lung disease
|
disease of the respiratory tract that produce an obstruction to airflow and affects mechanical function and gas exchange
|
|
|
How is the dx of obstructive lung distance confirmed
|
-Abnormal FEV1
-Decrease in expiratory flow rates and an increase in residual volume -Decrease in vital capacity and expiratory reserve volume |
|
|
Define COPD characteristics
|
by airflow limitation that is not fully reversible. The airflow limitation is usually progressive and associated with abnormal inflammatory response of the lungs to noxious particle or gases
|
|
|
For COPD where does the chronic inflammation happen
|
throughout airways, parenchyma, and pulmonary vasculature
|
|
|
How does inflammation occur in the central airways
|
Inflammatory cells infiltrate surface epithelium
|
|
|
How does inflammation occur in the peripheral airways
|
Repeated injury and repair increases collagen content/scar tissue formation
|
|
|
In COPD what cases airflow limitation
|
Loss of elastic recoil and fibrosis and narrowing of small airways, edema of airway, accumulation of secretions, and smooth muscle contraction
|
|
|
When and why does preamature airway collaspse
|
-when intrathoracic pressure in increased during active expiration -alveoli lose their elasticity, supportive structures are lost, reduced airway tethering
|
|
|
Incomplete lung emptying
|
dynamic lung hyperinflation
|
|
|
population for COPD vs population for asthma
|
elderly, especially smokers vs all ages including children
|
|
|
T/F: asthma is slowly progressive
|
False: COPD slowly progressive, asthma episodic course
|
|
|
Types inflammatory cells COPD vs asthma
|
-COPD=Neutrophils, macrophages, CD8+ cells
-Asthma= Eosinophils, mast cells, CD4+ cells |
|
|
T/F: COPD is completely reversible
|
partially reversible, and asthma is fully reversible
|
|
|
what are the three main components of COPD
|
inflammation, structural changesm bronchoconstriction
|
|
|
With COPD Inflammation is usually caused by
|
cigarette smoking causes airway inflammtion (neutrophils, macrophages, lymphocytes) even before symptoms occur
|
|
|
With COPD structural changes that occur
|
as the disease advances, small airways narrow as a result of inflammation and fibrosis and destructive changes of emphysema affect the lung parenchyma
|
|
|
With COPD why does bronchoconstriction occur
|
occurs with exposure to respiratory irritants and viruses and usually responds to bronchodilator therapy
|
|
|
what are the physiological changes
|
-narrowing and obstruction of airways
-inflammation of mucosal lining of bronchi and bronchioles -ciliary dysfunction -destruction of alveolar and bronchial walls -mucosal thickening -increased production and retention of mucus -spasm of bronchial smooth muscle -pulmonary hyperinflation -structural change in bronchioles -alveolar ventilation reduced -ventilation-perfusion mismatching -decreased gas exchanged -chronically elevated carbon dioxide levels -chronically low oxygen levels |
|
|
How does decreased gas exchange occur in COPD
|
-increased alveolar sac size with trapped air breaking down alveoli and septal walls
-less surface area for ventilation-perfusion |
|
|
In a normal person, what is the "drive to breathe"
|
regulated and pushed by the level of CO2 in blood stream; when the CO2 levels gets too high we take a breath and push some of that out
|
|
|
In COPD, what is the "drive" to breathe
|
regulated by the amount of O2 in the blood stream. When the level of O2 gets too low then the body is stimulated to take a breath
|
|
|
Why is it "bad" to give a pt with COPD oxygen
|
the O2 can raise the blood O2 levels to the point that the brain will think "Ok there is enough O2, so know I don't need to breathe"
|
|
|
What can chronically lox oxygen levels contribute to
|
-polycythemia
-increased blood viscosity -increased work of the heart |
|
|
What can chronically lox oxygen levels lead to
|
-pulmonary hypertension
-cor pulmonale |
|
|
what are risk factor that the patient may have
|
-genes= hereditary deficiency of alpha-1antitrypsin
-airway hyperresponsiveness |
|
|
what are risk factors that the patient may be exposed to
|
-tobacco smoke
-occupational dusts and chemicals -outdoor and indoor air pollution -infection (h/o respiratory infection) |
|
|
What are patient problems that the patient may have who have a pulmonary disease
|
-chronic cough
-excess sputum -wheezing -dyspnea on exertion -increased use of accessory muscles -decreased exercise tolerance -frequent respiratory infections -early morning headaches -associated postural defects |
|
|
What are patient problems that the patient may have who have a systemic disease
|
-Poor nutrition; weight loss
-Hypoxemia -Skeletal muscle dysfunction -Cardiovascular disease -Depression -Osteoporosis -Anemia of chronic disease |
|
|
What are the diagnostic test done for pts with pulmonary dysfunction
|
-Chest X-ray
-ABGs -pulmonary function tests -breath sounds -symptoms |
|
|
If a pt has a pulmonary dysfunction, what may come up on the following diagnostic test:
Chest X-ray |
-depressed diaphragm
-hyperinflation |
|
|
If a pt has a pulmonary dysfunction, what may come up on the following diagnostic test:
ABG's |
Decreases in PO2, increase in PCO2
|
|
|
If a pt has a pulmonary dysfunction, what may come up on the following diagnostic test:
Pulmonary function test |
post bronchodilator FEV1/FVC <0.7 confirms presence of decline in airflow that is not fully reversibe
|
|
|
If a pt has a pulmonary dysfunction, what may come up on the following diagnostic test:
Breath sounds |
distant or difficult to hear
|
|
|
If a pt has a pulmonary dysfunction, what may come up on the following diagnostic test:
symptoms |
increasing and/or abnormal SOB
|
|
|
What are the goals of treatment for pts with pulmonary COPD
|
-Improve breathlessness/relieve symptoms
-Improve lung function -Improve exercise tolerance -Prevent any further loss/disease progression -Prevent and treat complications/exacerbations -Smoking cessation! |
|
|
what is the pharmacological management of pts with COPD
|
-bronchodilator therapy
-anti-inflammatory agents -antibiotics |
|
|
What can lead to bronchoconstriction
|
abnormal bronchomotor tone (bronchospasm), inflammation, and/or mechanical obstruction
|
|
|
What bronchodilators are used for pulmonary dysfunction
|
Anticholingerics
Beta2 Agonists Methylxanthines |
|
|
What anti-inflammatory agents are used for COPD for pulmonary dysfunction
|
Cromolyn sodium
Corticosteriods Inhaled Oral |
|
|
when should oxygen be used
|
if during exercise SaO2 goes down when then had SaO2 of 90% or more
|
|
|
When is long term use of supplemental oxygen indicated
|
PO2<55mmHg (SaO2 of <88%), in order to prevent tissue hypoxia
|
|
|
What is lung volume reduction therapy
|
removal of portions of nonfunctional lung to reduce hyperinflation
|
|
|
What are the precautions of lung volume reduction therapy
|
no resistive strengthening exercises (push-ups, pull-ups) to involved UE although full ROM is encouraged for 6 weeks
|
|
|
what is the PT for a pt after lung volume reduction therapy
|
breathing exercise, coughing/splinting, early mobilization
|
|
|
when is lung transplantation used
|
for end-stage pulmonary disease
|
|
|
what are the goals after lung transplantation
|
restore normal lung function and exercise capacity and prolong life
|
|
|
What does PT work on post-op after lung transplantation
|
-Breathing exercises, coughing/splinting techniques, patient positioning, pain reduction, early mobilization
-Education |
|
|
What is going to be part of pt education after lung transplantation
|
-signs of potential rejection or infection
-side effects of steriods -self-monitoring and progression of endurance and strengthening program |
|
|
what are the side effects of steriods
|
-proximal muscle weakness
-decreased bone density -depression, emotional lability, change in affect or mood -difficulty sleeping -tremor or incoordination -cushinoid feature -slowed wound healing |
|
|
what is the purpose of aerobic exercise training
|
improve exercise capacity of pts, QOL, dyspnea
|
|
|
How does skeletal muscle function decrease in patients with pulmonary dysfunction
|
-decreased mm mass, strength, endurance
-develop lactic acidosis as lower exercise workloads |
|
|
what does the American thoracic society recommend
|
walking, 20-30 min, 2-5x/week, intensity 60% of VO2 max when possible
|
|
|
FITT for Mild COPD or well-controlled asthma for aerobic capacity
|
**Make sure adequate warm-up and cool-down periods
F=3-5 d/week I=older adults T=20-60min/day of continuous or intermittent physical activity T=walking |
|
|
FITT for moderate to Severe COPD for aerobic capacity
|
**Make sure adequate warm-up and cool-down periods
F=3-5 d/week I= 60-80% of peak work rates T=starting off may only be a few minutes, so may do intermittent until build tolerance and endurance T=walking |
|
|
How can you measure the intensity of aerobic exercise in moderate to severe COPD
|
-dyspnea ratings (moderate SOB to strong/hard breathing)
-RPE ratings 11-13 on 6-20 scale |
|
|
what should aerobic exercise training be done in junction with
|
pt education, pacing, energy conservation, breathing techniques, anxiety, and dyspnea management
|
|
|
T/F: aerobic exercise training improves inspiration muscle function
|
FALSE
|
|
|
When breathing at increased lung volumes what happens to the elastic work of breathing and respiratory muscles
|
the elastic work of breathing is increased and respiratory muscles are placed at mechanical disadvantage
|
|
|
what does exercising deconditioned muscles require
|
The increased metabolic demand from exercising deconditioned muscles requires increase minute ventilation
|
|
|
during exercise what usually increases minute ventilation
|
During exercise, the increased minute ventilation is usually via primarily an increased tidal volume, then an increased respiratory rate
|
|
|
what may cause the pt to breathe in before the preceding breath is fully exhaled
|
The combination of increased dyspnea, prolonged expiratory time, and increased respiratory rate
|
|
|
what contribues to exertional dyspnea of COPD
|
dynamic hyperinflation
|
|
|
What does exercise training in COPD indirectly reduces
|
dynamic hyperinflation by lower the respiratory rate during exercise—thus allowing for more complete lung emptying with each breath
|
|
|
what may be some clinical implications for PT in patients with pulmonary dysfunction
|
-Need to assess airway clearance, breathing patterns, chest wall and shoulder mobility, physiological responses to exercise
-Need to provide physiological monitoring during PT At least initially -Consider use of a bronchodilator before PT treatment as it may enhance exercise tolerance -Patients should never exercise on less oxygen than they use at rest ---PTs have a role in identifying if increased supplemental oxygen use is required during activity |
|
|
what are some treatment options for physical therapy for patients with COPD
|
-Facilitate effective cough and airway clearance
-Positioning for relaxation -Decrease use of accessory muscles -Encourage use of pursed-lip breathing ---Only breathing pattern that should be taught to patients with stable COPD -Decrease forward head/rounded shoulders; improve posture and chest mobility -Pt education/family education |
|
|
FITT for Resistance Training for pts with COPD
|
F=2-3 d/w
I=8-12 reps to fatigue per set of each exercise, 3 sets for all extremities and trunk T=graded endurance and aerobic |
|
|
what entails pt education about COPD
|
-about disease
-self-management -effects of smoking -nutrition -weight control -smoking reduction or cessation -stress management -other lifestyle factors -medications -infection control -role of a long term rehabilitation program |
|
|
what entails pt monitoring with COPD
|
-Dyspnea
-Respiratory distress -Breathing pattern (depth and frequency) -Arterial saturation -Cyanosis -HR -BP |
|
|
what is emphysema characterized by
|
-abnormal permanent enlargement of airspaces distal to the terminal bronchiole, accompanied by destruction of their walls
|
|
|
what causes the permanent enlargement of airspace that is characterized in emphysema
|
-Destruction of alveolar wall
-Proteolytic enzymes degrade elastin |
|
|
what are the characteristics of chronic bronchitis
|
-Increase in the size of the tracheobronchial mucous glands and goblet cell hyperplasia
-Decrease in number of cilia -In peripheral airways, bronchiolitis, bronchiolar narrowing, and increased amounts of mucus are observed |
|
|
How is chronic bronchitis diagnosed
|
-Cough producing sputum on most days for 3 months during 2 consecutive years when other conditions have been ruled out
--Chronic productive cough --Increased risk of respiratory infections |
|
|
what is asthma
|
-Acute and chronic inflammatory condition of the airways
-Increased responsiveness of the airway smooth muscle to various stimuli |
|
|
what is extrinsic asthma vs intrinsic
|
extrinsic=allergic
intrinsic=non-allergic |
|
|
what is the pathology of asthma
|
-Widespread narrowing of the airways that reverses either spontaneously or as a result of treatment
-During an attack, the lumens of the airways are narrowed or occluded by a combination of: --bronchial smooth muscle spasm, inflammation of the mucosa, and overproduction of viscous mucus -Eosinophilic inflammation is prevalent -Airway remodeling of the bronchial airways occurs over time |
|
|
what are the patient problems associated with asthma
|
-Cough with or without sputum production
-Dyspnea -Wheezing -Chest tightness -Tachypnea -Use of accessory muscles -Expiratory phase of breathing is prolonged -Early in attack, hypoxemia and low PaCO2 ---from hyperventilation -As attack progresses, low PaO2 and increase PaCO2 ---airtrapping |
|
|
medical management asthma
goals |
-maintenance of adequate arterial oxygen saturation
-relief of airway obstruction -reduction of airway inflammation -control symptoms -avoid known allergens and irritants |
|
|
what are the medications included with asthma
|
-inhaled steriods (flovent)
-Leukotrien inhibitors (Singulair) -Long acting bronchodilators (Serevent) -Combination of steroids and bronchodilators (Advair Diskus) -Cromolyn sodium (Intal) -Short acting bronchodilators (Proventil, Xopenex) -Corticosteriods |
|
|
when is corticosteriods used
|
for acute attacks
|
|
|
What is the PT management for asthma
|
-promote more effective and efficient breathing
|
|
|
What can a PT do in order to promote more effective and efficient breathing
|
-Relaxed controlled breathing maneuvers and controlled unforced coughing in optimal body positions
-Airway clearance techniques -Chest wall mobility exercises -Pt Education -Aerobic exercise |
|
|
What is include for pt education for promoting effective and efficient breathing?
|
-Stress management
-Activity pacing -Triggers -Preventative health practices (Nutrition, weight control, flu shots, smoking cessation, benefits of long term rehabilitation) |
|
|
what is cystic fibrosis
|
multisystem disorder transmitted by autosomal-recessive gene that effects exocrine glands
|
|
|
what is cystic fibrosis characterized by
|
-increased electrolyte content of the sweat, chronic airflow limitation, and pancreatic insufficiency
|
|
|
what are the physiological problems that are associated with cystic fibrosis
|
-Increased secretion of abnormally viscous mucus
-Impaired mucociliary transport resulting in airway obstruction -Bronchiectasis=(Chronic dilation of the bronchial tubes) -Hyperinflation -Infection -Impaired regional ventilatory function -Impaired ventilation and perfusion matching and gas exchange |
|
|
Medical management of cystic fibrosis
goals for acute exacerbation of CF |
-enhance mucociliary transport
-promote airway clearance -optimize alveolar ventilation -gas exchange -maximize the efficiency of oxygen transport overall -prevent and minimize infection |
|
|
Medications for cystic fibrosis
|
-Antibiotics
-Inhaled beta2 agonist bronchodilators -Inhaled hypertonic saline -DNAse enzyme replacement therapy -Ibuprofen (children 5-13) |
|
|
what is inhaled hypertonic saline used for
|
To increase hydration of airway surface liquid to improve mucociliary clearance
|
|
|
What is the purpose Ibuprofen
|
May slow lung deterioration in some children
|
|
|
PT management of cystic fibrosis
|
-Airway clearance techniques
-Breathing control/exercises and coughing/huffing -Chest wall mobility exercises -Mobilization -Aerobic conditioning -Education of patient/caregiver in chronic care needs |
|
|
PT education of a patient with cystic fibrosis
|
-Relaxation
-pacing -energy conservation |
|
|
What is restrictive lung dysfunction
|
Abnormal reduction in pulmonary ventilation
|
|
|
what is restrictive lung dysfunction caused by
|
Lung expansion diminished
Decreased volume of air into/out of lungs |
|
|
restrictive lung dysfunction is usually a result of what
|
extrapulmonary or pulmonary restriciton
|
|
|
what are the physiological changes that occur the restrictive lung dysfunction
|
-Decreased lung expansion
-Decreased pulmonary compliance -Increased work of breathing -Decreased tidal volume, inspiratory and vital capacities, total lung capacity -Ventilation-perfusion mismatching |
|
|
Patient problems or impairments with restrictive lung dysfunction
|
-Difficult to take a deep breath
-Tachypnea -Dypsnea -Irritating, dry, non-productive cough -Increased use of accessory muscles -Decreased thoracic mobility -Postural changes -General weakness and fatigue |
|
|
Dx test for restrictive lung dysfunction
|
-chest X-rays
-ABGs -pulmonary function test -breath sounds (dry crackles) |
|
|
what is the medical management of restrictive lung disease
|
depends on the etiologic factors, if they are permanent or progressive in nature than treatment is supportive
|
|
|
what is the pharmacological management of restrictive lung disease
|
-Antibiotics
-Anti-inflammatory agents |
|
|
what are some surgical management methods available for restrictive lung disease
|
Chest tubes
Lobectomy or wedge resection (lung CA) Lung transplantation |
|
|
what is the medical management of restrictive lung disease
|
-medication
-supplemental oxygen -surgical manangement |
|
|
What are the clinical implications for PT for restrictive lung disease
|
Need to assess airway clearance, breathing patterns, chest wall and shoulder mobility, physiological responses to exercise
|
|
|
what is the relationship between restriction and respiratory rate
|
The more severe the restriction, the more dependent the patient will be on respiratory rate as the only means to increase minute ventilation during exertion
|
|
|
what are the PT treatment options available for pts with restrictive lung diesase
|
-Facilitate effective cough
-Airway clearance techniques -Decrease use of accessory muscles -Increase diaphragmatic breathing, lateral costal and segmental expansion -Chest and UE mobilization -Improve postural deficits -Educate on energy conservation, work simplification, and pacing techniques -Graded endurance and aerobic activities |
|
|
What are the specific restrictive lung conditions for extrapulmonary restrictions
|
Chest wall injury
Structural abnormalities Postural deformities Respiratory muscle weakness Obesity or ascites |
|
|
What are the specific restrictive lung conditions for pulmonary restrictions
|
Disorders of lung parachyma and pleura
Disorders of cardiovascular origin Normal aging |
|
|
what are examples of disorders of lung parachyma
|
-tumor, cancer
-interstitial pulmonary fibrosis -atelectasis |
|
|
what are examples of interstitial pulmonary fibrosis
|
-pneumonia
-TB |
|
|
what are disorders of cardiovascular origin
|
-pulmonary edema
-PE |
|
|
what is atelectasis
|
-partial collapse of lung parenchyma
|
|
|
what are some causes of atelectasis
|
-Breathing too shallow
-Respiratory muscle weakness -Mechanical ventilation -Physical compression of the lung -Obstruction of an airway |
|
|
what are some patient problems that come up with atelectasis
|
-decreased chest wall movement and decreased breath sounds over involved area
-chest x-ray increased density over involved area -may see tachypnea, cyanosis |
|
|
PT management of a pt with atelectasis
|
-Preventative management of patient
-Mobilization -Positioning to optimize alveolar ventilation -Breathing control/exercises and coughing (slide 65) |
|
|
Why does pneumonia occur
|
when the normal defense mechanisms of the respiratory system fail to adeuquately protect the lungs from infection
|
|
|
what are major routes of infection for pneumonia
|
airbourne organism, circulation, contigous infection, aspiration
|
|
|
What are the patient problems associated with pneumonia
|
-fever
-tachypnea -dyspnea -hypoxiea -loss of appetite -cough -chest x-ray |
|
|
what is the PT management for a pt with pneumonia
|
-mobilization
-positional changes -airway clearance -breathing control/exercise and coughing -education on pacing of activities |
|
|
what is the purpose of positional changes
|
maximize alveolar ventilation, mucociliary transport and gas exchange
|
