Chronic Obstructive Pulmonary Disease Flashcards
What is COPD characterized by?
What is it often accompianed by?
What are its major disorders? 4
What is the only thing that really helps in treating non reversible COPD?
Characterized by decreased airflow rate during expiration.
Often accompanied by elevated functional residual capacity resulting from trapped air.
Major Disorders:
- COPD
- Chronic Bronchitis
- Emphysema
- Bronchiectasis
Supplemental oxygen
Chronic bronchitis is defined by what?
a chronic productive cough for three months in each of two successive years in a patient in whom other causes of chronic cough have been excluded.
(They will fit the picture)
Emphysema is defined by what?
2
- abnormal and permanent enlargement of the airspaces that are distal to the terminal bronchioles.
- This is accompanied by destruction of the airspace walls, without obvious fibrosis (less muscus)
Bronchiectasis shares many clinical features with COPD, including what?
3
What infections are often associated with this?
2
- inflamed and easily collapsible airways and
- obstruction to airflow usually caused by infection.
- (outpouchings with lots of mucus getting stuck in there)
- pseudomonas
- staff
WHO’s defintion of COPD?
3
What does a heart sound like with COPD?
characterized by airflow limitation that is not fully reversible. The airflow limitation is usually progressive and associated with an abnormal inflammatory response of the lungs to noxious particles or gases.”
- Not fully reversible
- progressive
- abnormal inflammatory response
Not much. Will have large AP area and a lot of air trapped in there. But they will probably have heart disease so you cant miss it.
AGAIN! What is COPD characterized by?
Periodic exacerbations are caused by what?
3
Slow, progressive irreversible airway obstruction due to chronic bronchitis and/ or emphysema
Periodic exacerbations with:
- Increased dyspnea
- Increased sputum (usually colorless)
- Occasionally respiratory failure
Describe the onset of COPD?
What is the most frequent cause of COPD?
What will help us identify susceptible patients?
Takes years to become clinically significant.
Cigarette smoking is the most frequent cause, although fewer than 1 in 5 smokers will develop the disease.
Signs of airflow obstruction on PFT’s can identify susceptible patients.
Known Risk factors for COPD:
Agent? 2
Host? 1
- Cigarette Smoke
- Environmental/Occupational dusts and gases
- Alpha 1 antitrypsin deficiency
Probable risk factors for COPD:
Agent? 5
Host? 4
- Air pollution
- Passive (involuntary) smoking
- Respiratory viruses
- Socioeconomic factors/living conditions
- Alcohol
- Age
- Gender
- Familial/genetic
- Airway hyperresponsiveness
Where is the site of airway obstruction in COPD?
This results in peripheral airway resistance due to:
3
Muscus buildup occurs why?
in the smaller conducting airways ( less than 2mm in diameter)
- Destruction of alveolar support
- Loss of elastic recoil
- Structural narrowing due to inflammation
outpuchings created by inflammation?
What volumes and capacities are increased in COPD? 3
What is reduced? 1
What is this due to? 4
- Residual volume and
- functional residual capacity are increased.
- Total lung capacity may remain normal but is often increased.
- Vital capacity is reduced:
- Due to air trapping
- Decrease in lung elastic recoil
- Demands for increased minute volume may not allow the lungs to empty completely during the time available for expiration
- end stage airway collapse
What process in the pathphysiology of COPD causes ventilation/perfusion mismatch? 3
What process stops perfusion and creates a physiological dead space? 3
Metabolic costs of breathing become excessive and cause?
- Loss of surface area along with
- bronchial obstruction and
- altered distribution of ventilated air
- Hyperinflation of the lungs, in which
- alveolar pressure exceeds pulmonary artery pressure
- stops perfusion and creates a physiologic dead space.
respiratory muscle fatigue
- Structural changes ______ the work of breathing.
- What kind of lung volumes put inspiratory muscles at a mechanical disadvantage?
- Diaphragm is ______, _______ its ability to change intrathoracic volume.
- Destruction of alveoli affects gas exchange how?
- WHy are these important features?
- Why do we want to treat aggressively?
- increase
- Larger
- flattened
decreasing - decreases surface area for gas exchange.
- They are easily recognizable on a chest X-ray
- Because everytime they have an exacerbation they because even more immunocomprimised and it will happen more frequently
What is asthma characterized by?
5
- variable and recurring symptoms,
- airflow obstruction,
- bronchial hyper-responsiveness and an
- underlying inflammation.
- Reversible
What are the three airway limitations in asthma patients?
3
What test will define whether its asthma or COPD?
What cells are affected in asthma (2) and which are affected in COPD (3)?
Bronchoconstrction
Airway hyperresponsiveness
Airway edema
Bronchodilator challenge
Asthma- CD4, eosinophils
CD8, macrophages and neutrophils are COPD
Describe what the following terms are:
Bronchoconstrction
Airway hyperresponsiveness
Airway edema
Bronchoconstriction
—Bronchial smooth muscle contraction in response to exposure to a variety of stimuli
Airway hyper-responsiviness
—-Exaggerated bronchoconstrictor response to stimuli
Airway edema
—-Edema, mucus hyper-secretion, formation of thickened mucus plugs
Chronic Bronchitis (blue bloaters) is defined as?
The pathologic findings include the following. 3
What do the patients look like?
Defined as a persistent cough resulting in sputum production for more than 3 months in each of the past 2 years.
- Goblet cell hyperplasia
- Mucus plugging, excess mucus secretion
- Fibrosis
Barrel chested, blue because there is so little oxygen. men usually
- Pathological findings, along with loss of supporting alveolar, cause what?
- Excessive bronchial secretions and airway obstruction cause what?
- Blue bloaters are unable to maintain ______ by increasing their breathing effort.
- ______, ______, and ________ develop earlier than emphysema
- Have a greater chance of developing what?
- airflow limitation due to airway wall deformities thus narrowing the airway lumen.
- a ventilation/perfusion mismatch.
- normal blood gases
- Hypoxemia, hypercapnia and cyanosis
- Cor Pulmonale
COPD
Chronic Bronchitis
Classic symptoms?
4
- Increasingly productive cough
- Dyspnea with a progressive decrease in exercise tolerance
- Frequent and recurrent pulmonary infections
- Weight gain
Defintion of Emphysema (pink puffers)?
4
- Abnormal enlargement of the airspaces distal to the terminal bronchioles,
- with destruction of the alveolar walls and capillary beds
- Abnormal airspaces called Bullae compress surrounding area of more normal lung
- Loss of lung elasticity
What are the most common causes of emphysema?
Whats the difference between pink puffers and blue bloaters?
- cigarette smoking and
- Alpha-1 Antitrypsin Deficiency.
pink puffers still have a equal match of perfusion and ventilation (fighters)
Blue bloaters can ventilate (non fighters)
Long history of progressive 1. ______ w/late onset of 2. _______ ______. Patients don’t realize they have it until well into later stages of the disease.
Initially, they are able to 3. _________ and maintain relatively normal blood gas levels until late in the disease.
The work of breathing makes 4. _____ difficult. Patients are usually 5. _____.
- dyspnea
- nonproductive cough
- overventilate
- eating
- cachectic (little old lady who is wasted away/skinny because she isnt eating. cant breath)
Pursed lip breathing is helpful for COPD Emphysema. Why?
2
- Increases resistance to the outflow of air
2. Helps to prevent airway collapse by increasing airway pressure
WHat will happen to the pulmonary vessels of COPD pats?
They will constrict. This will continue to narrow the blood supple and cause right side hypertrophy.
Most common early symtpom of COPD?
exertional dypsnea (will go through a cardiac workout to rule that out)
What are the two types of emphysema?
Centrilobular emphysema (CLE) Panlobuar emphysema (PLE)
Why is the Alpha-1 Antitrypsin Deficiency pathogenic?
Alpha-1 Antitrypsin blocks the other kind of enzymes that are working to break down the alveoli. Without it they are not protected
- WHats the most common type and what is it characterized by?
- Seen mostly in who?
- Most severe in what part of the lungs?
- Centrilobular emphysema
Most common type
Characterized by focal destruction - Seen predominately in male smokers
- Most severe in the upper lobes
What does Panlobular emphysema involve?
Where is it most severe?
Most commonly seen in what kind of pts?
Involves the entire alveolus distal to the terminal bronchiole
Most severe in the lower lung zones
Generally develops in patients with homozygous alpha1-antitrypsin (AAT) deficiency
What will we see in the specimen of an Emphysematus Lung?
large air spaces
How is Alpha-1 Antitrypsin Deficiency aquired?
WHo do we need to watch out for with this?
Congenital
Should be considered in younger patients who show signs of emphysema, whether they have smoked or not.
What is Alpha-1 Antitrypsin?
2
In healthy persons, alpha1-antiprotease serves as a protective screen that prevents alveolar wall destruction.
The imbalance of proteases-antiproteases in the alveolus leads to unimpeded neutrophil elastase digestion of elastin and collagen in the alveolar walls and progressive emphysema.
COPD Emphysema work up
Lab studies? 1
Imaging? 2
Lab Studies:
1. Serum alpha1-antitrypsin levels
Used to identify disease and determine serum alpha1-antitrypsin (AAT) levels.
Phenotyping is required to confirm AAT deficiency. Do not initiate AAT replacement therapy without testing.
- Chest radiography:
AAT deficiency emphysema produces a hyperlucent appearance because healthy tissue has been destroyed. - Chest CT: Demonstrates widespread abnormally hypoattenuating areas resulting from a lack of lung tissue
COPD Emphysema
Treatment?
- Prolastin
AAT-deficient individuals who have or show signs of developing significant emphysema can be treated with Prolastin, a pooled, purified, human plasma protein concentrate replacement for the missing enzyme. The US Food and Drug Administration (FDA) has approved 2 other AAT protein concentrates, Aralast and Zemaira, for augmentation therapy.
Weekly IV infusions of AAT protein concentrates restore serum and alveolar AAT concentrations to protective levels. Although other dosing regimens have been used, only the weekly infusion schedule has US FDA approval.
Physical signs of COPD
9
- Increased anteroposterior chest diameter (barrel chest)
- Use of accessory muscles to breathe
- Peripheral cyanosis
- Clubbing of the fingernails (a sign of chronic hypoxia)
- Decreased breath sounds
- Hyperresonance on percussion
- Wheezing on expiration
- Prolonged expiratory phase
- Low, flat diaphragm
In advanced COPD what will you find?
10
- Intervals between exacerbations become shorter
- Cyanosis
- Significant hypoxia and hypercapnea
- Polycythemia - erythocytosis
- Pulmonary hypertension
- Right ventricular hypertrophy
- Right sided heart failure (Cor Pulmonale)
- JVD
- Peripheral edema
- Hepatojugular reflex
What are the key indicators for COPD?
5
- Chronic cough
- Chronic sputum production
- Dyspnoea that is
- Acute bronchitis
- History of exposure to risk factors
Describe what the following with be like in COPD pts?
- Chronic cough
- Chronic sputum production
- Dyspnoea that is
- Acute bronchitis
- History of exposure to risk factors
- Present intermittently or every day often present throughout the day; seldom only nocturnal
- Present for many years, worst in winters. Initially mucoid – becomes purulent with exacerbation
- Progressive (worsens over time)
Persistent (present every day)
Worse on exercise
Worse during respiratory infections - Repeated episodes
- Tobacco smoke, occupational dusts and chemical smoke from home cooking and heating fuel
What will we see on a COPD chest Xray?
4
What might you miss if you dont do an X-ray?
- Hyperinflation
- Flattening of the diaphragm
- Increased retrosternal air space
- Long narrow heart shadow
Might miss cancer (they are at a high risk)
In early stages what will ABGs show?
With the progression of the disease what becomes more prominant?
With a lower pH what does this cause?
ABG’s show mild to moderate hypoxia without hypercapnia in early states.
With progression of disease, hypercapnia becomes more prominent
Lower pH with renal compensation.
What will the ABG look like: pH pCO2 PO2 HCO3
pH - 7.35
pC02 - 75
P02 – 60
HCO3 - 32
PFT’s are the cornerstone of making the DX:
What will we see changed?
4
What will the EKG show?
- FEV1 decreased
- TLC, FVC and RV increased
- Carbon dioxide diffusing capacity is decreased
- No reversibility with bronchodilators like asthma!
Electrocardiogram may show right ventricular hypertrophy (RVH)
What is cor pulmonale? 2
What are the complications with this?
5
- Pulmonary Hypertension and
- Right sided heart failure
- Poor gas exchange
- Lower O2 level in blood
- Constriction of the blood vessels
- Right ventricular hypertrophy (RVH)
- Loss of contractile efficacy
COPD complications
5
- Cor pulmonale
- Pneumonia
- Pneumothorax
- Secondary polycythemia
- end stage lung disease
What is the most common infection for COPD? (what should we treat with?)
What will be see if they develop a pneumothorax? 2
What is happening when they get secondary polcythemia? 1
Pneumonia
- Strep pneumoniae most common.
- Augmentin
Pneumothorax
- Bullae
- Weakened lung structure
Secondary Polycythemia
1. Body increases production of O2-carrying RBC’s to compensate.
How will end stage lung disease present?
4
- Respiratory failure
- Decline in lung function
- Rising levels of CO2 in blood
- Eventually leads to slow loss of consciousness and cessation of breathing
COPD–Treatment
7
- Smoking cessation!!!
- Pulmonary rehab
- Respiratory muscle conditioning
- Whole body conditioning and strengthening
- Breathing training
- Immunizations
- Medications
Pharmacotherapy for Stable COPD? 2
Bronchodilator
Steriod
What kind of bronchodilator can we use?
4
- Short-acting β2-agonist – Albuterol!!!!!!!!!!!
- Long-acting β2-agonist - Salmeterol (Serevent) and Formoterol (Foradil)!!!!!!!!!
- Anticholinergics – Ipratropium (Atrovent), Tiotropium (Spiriva)
- Methylxanthines - Theophylline
What kind fo Steriods would we use?
2
- Oral – Prednisolone
2. Inhaled – Fluticasone (Flovent), Budesonide (Endocort)
What do Anticholinergics also help with?
sputum produciton
How should we prescribe the these medicines together?
4
Bronchodilators
1. As needed short-acting inhaled bronchodilators
Beta 2 agonists: albuterol
Anticholinergics: ipratropium (Atrovent)
IMPORTANT that the patient knows how to use them properly and when to use them
- Give both bronchodilators together
- Long-acting inhaled bronchodilators
Salmeterol (Serevent)
Tiotropium (Spiriva)
Or Theophylline (not used much because of SE and need to draw levels) - Corticosteroids
Inhaled 1st (Advair) What do patients need to do after using?
Systemic for severe exacerbations
Bronchodilator medications are central to the symptomatic management of COPD. They are given on an as-needed basis or on a regular basis to do what?
The principal bronchodilator treatments are what (3) used singly or in combination.
Regular treatment with _____-acting bronchodilators is more effective and convenient than treatment with ____-acting bronchodilators
prevent or reduce symptoms and exacerbations.
beta-agonists, anticholinergics, and methylxanthines
long
short
Combined therapy LABA + ICS resulted in:
5
- Reduced exacerbation rates
- No significant difference in the rate of hospitalizations.
- Mortality was also lower with combined treatment.
- Improved quality of life,
- lung function improvement and better compliance.
A benefit of usuing Mucolytics - Mucomyst was seen in what kind of patients?
2
- who have frequent or prolonged exacerbations, or
2. those who are repeatedly admitted to hospital with exacerbations with COPD.
They should be considered for use, through the winter months at least, in patients with moderate or severe COPD in whom ________ ________ are not prescribed.
inhaled corticosteroids (ICS)
Long term oxygen therapy is the only treatment that has been shown to prolong survival.
Patients with the following should have long term continuous oxygen therapy?
Decreases risk of?
3
O2 sat below 90%
- Right sided heart failure
- Polycythemia
- Impaired mental status
Why cant we put them on more oxygen than they need?
We would stop their ventilatory drive which is controled by CO2 levels
Benefits of oxygen?
4
- Less dyspnea
- Improved functional capacity and quality of life
- Improvement in pulmonary hypertension
- Prolonged survival
How many hours a day do they need to be on it to be beneficial?
Who will supplemental not help?
To benefit must use close to 24 hours per day
at least >15 hours per day
No benefit if O2 saturation is not low
Non-pharmacological therapy?
3
- Whole body conditioning/exercise
- Nutrition (imporve protein status and weight gain)
- Pulmonary rehabilitation
Why is pulmonary rehab important?
2
- Relieves dyspnea and fatigue.
2. Improves emotional function and enhances patients’ sense of control over their condition.
Treatment options for Severe COPD?
2
- Lung reduction surgery for emphysema
5 to 20% mortality
86% mean improvement in FEV1 at 6 months
Benefits may be lost by 5 years - Lung transplant
What is the goal of Lung Volume Reduction Surgery (LVRS)?
3
- The goal of the surgery is to reduce the size of the lungs by removing about 20-30% of the most diseased lung tissues so that the remaining healthier portion can perform better.
- allows the diaphragm to return to its normal shape, allowing the patient to breathe more efficiently.
- reduce overall lung volume
Guidelines for Referral: Describe
BODE index exceeding 5
4
BODE takes into account
- body mass index,
- airway obstruction (as measured by FEV1),
- dyspnea (as measured by the MMRC dyspnea scale) and
- exercise tolerance (as measured by the 6 minute hall walk test).
In addition, researchers say the BODE Index is a better predictor of COPD mortality than FEV1 alone.
Guidelines for Transplantation
Patients with a BODE index of 7 to 10 and at least 1 of the following?
3
- History of hospitalization for exacerbation associated with acute hypercapnia (PCO2 exceeding 50 mm Hg)
- Pulmonary hypertension or cor pulmonale, or both, despite oxygen therapy
- FEV1 of less than 20% and either DLCO of less than 20% or homogenous distribution of emphysema
Describe acute exacerbations?
It may or may not be accompanied by 3
considered to be episodes of increased dyspnea and cough and change in amount and character of sputum.
- fever,
- myalgias and
- sore throat.
How do we approach assessment of the exacerbation?
3
Approach to the patient includes assessment of
- severity ,
- identification of the precipitating factor and
- institution of therapy.
Three precipitating causes of exacerbaitons?
- Bacterial infections play a role in many episodes.
- Viral infections are involved in 1/3 rd of cases.
- In 20 – 35% no specific precipitant can be identified
Most common Bacterial infections that cause exacerbation? 4
Viral? 2
(H.influenzae, S.pneomoniae, M.catarrhalis and Mycoplasma)
Influenza and Adenovirus
PATIENT ASSESMENT
History should include questions in regards to:
5
- Dyspnea during activities and at rest
- Fever
- Change in character of sputum
- Associated symptoms as nausea, vomiting, diarrhea, myalgias and chills.
- Inquire about frequency and severity of previous exacerbations.
Tests to order for patient assessment for COPD? 3
CXR, CBC and possibly ABGs
INSTITUTION OF THERAPY
What should we give them?
4
Oxygen
Inhaled Bronchodilators
Glucocorticoids
Antibiotics
What are our oxygen goals?
2
- achieve and maintain PaO2 > 55-60 mm Hg and
2. to keep arterial saturation > 90%.
INDICATIONS FOR ICU ADMISSION
6
- SEVERE DYSPNEA
- MENTAL STATUS CHANGES
- PERSISTENT WORSENING
- HYPOXEMIA
- HYPERCAPNIA
- RESPIRATORY ACIDOSIS
DISCHARGE CRITERIA
3
Use of inhaled bronchodilators less frequently than every 4 hrs.
Clinical and ABG stability for at least 12 – 24 hrs.
Acceptable ability to eat , sleep and ambulate.
Bronchiectasis
Requires 2 factors for diagnosis
- Infectious insult
2. Impaired drainage, airway obstruction or defect in host defense
Host response to insult or blockage results in what? 3
What does this cause? 4
the release of
- immune effector cells,
- neutrophilic proteases, and
- inflammatory cytokines
These cause
- transmural inflammation,
- mucosal edema,
- ulceration, and
- neovascularization in the airways
What is the result of bronchiectasis? 2
What is common?
- permanent abnormal dilatation and
- destruction of the major bronchi and bronchiole walls
Recurrent infection is common which feeds into the cycle of further scarring, obstruction, and distortion of the airways along with temporary or permanent damage to the lung parenchyma
Bronchiectasis:
1. An abnormal destruction and dilatation of the _____ ______.
- Describe how it can be caused?
- In bronchiectasis, the diameter of the bronchi is unusually _____.
- Examination of the walls of the bronchial tubes reveals WHAT , with replacement by WHAT. (remodeling)
- ___ collects within the bronchi, and WHAT is impaired.
- large airways
- Congenital or acquired.
- large
- destruction of the normal structural elements
- Scar tissue
- -Pus
- -the normal flow of oxygen into the lungs, and carbon dioxide out of the lungs
Bronchiectasis–Etiologies
Causes?
6
- Often caused by recurrent inflammation or infection of the airways.
- It may be present at birth, but most often begins in childhood as a complication from infection or inhaling a foreign object.
- Defective host defenses
- Recurrent, severe lung infections (pneumonia, tuberculosis, fungal infections)
- Obstruction of the airway by a foreign body or tumor
- Can also be caused by routinely breathing in food particles while eating (reflux)
Bronchiectasis—Presentation
Describe the onset of symtpoms?
What are the symtpoms?
11
Symptoms often develop gradually and may occur months or years after the event that causes the bronchiectasis.
Symptoms
- Chronic cough with large amounts of foul-smelling sputum production
- Hemoptysis
- Cough worsened by lying on one side
- Shortness of breath worsened by exercise
- Weight loss
- Fatigue
- Clubbing of fingers may be present
- Wheezing
- Cyanosis
- Paleness
- Halitosis
Bronchiectasis—Diagnosis
What would we hear on auscultaion?
Work up may include:
8
May hear small clicking, bubbling, wheezing, rattling, or other sounds, usually in the lower lobes of the lungs.
- Chest X-ray
- Chest CT - particularly good at revealing the thick, dilated bronchial walls of bronchiectasis.
- Sputum culture
- CBC, may reveal anemia and differential may show evidence of left shift or fungal infection
- A sweat test or other cystic fibrosis testing
- Serum Immunoglobulin analysis for cystic fibrosis or immune dysfunction in host
- Serum precipitins (testing for antibodies to the fungus aspergillus)
- A PPD (purified protein derivative) skin test for prior TB infection
Bronchiectasis—Treatment
5
Treatment should involve efforts to resolve any underlying disorder and improving bronchial hygiene.
- Antibiotic therapy for the appropriate organism. Other medications are of questionable benefit.
- Obstruction may require the removal of a foreign object or tumor.
- Mucolytics are indicated to help thin the sputum, so that it can be more effectively expectorated and to treat infections appropriately.
- Physiotherapy - Percussion and postural drainage may help the lungs to drain more effectively.
- Surgery is indicated when a particular area of the lung is constantly and severely infected.
Bronchiectasis - Treatment
ANTIBIOTIC THERAPY:
Used to treat acute exacerbations, to prevent infection or to reduce bacterial burden. What are the three strategies with antibiotics?
1 – High oral dose for prolonged period Zithromax 500mg 2/wk for 6 months
2 – Aerosolized antibiotic Gentamyacin 40mg BIDx x 3 days/4 wks
3 – Regular pulsed dose of IV antibiotics – 2-3 week courses with 1-2 months in between
Non antibiotic treatments for bronchiectasis?
4
- Pneumococcal and influenza vaccination
- ICS – Fluticasone (Flovent) BID
- NSAIDS – significantly slowed progression of disease in CF-bronchiectasis
- Pulmonary rehab improved exercise tolerance but simultaneous inspiratory muscle training offered not additional benefit.
