COPD, Asthma, and Obstructive Disorders

Question 1

How does pneumonia effect gas exchange in the alveoli?

Answer 1

• Decreases surface area
• increases distance over which diffusion must occur
• both of these result in less effective gas exchange

Question 2

Respiratory pathophys of pneumonia:

Answer 2

• swelling narrows airway, decreasing airflow

- mucus increases, reducing air space

Question 3

Respiratory pathophys of bronchitis:

Answer 3

-narrows bronchial tubial= less air flow

Question 4

Chronic Obstructive Pulmonary Disease (COPD)

Answer 4

characterized by airflow limitation and encompasses several subtypes of obstructive airway disease; chronic bronchitis, emphysema and asthma*

• affects 32 million ppl each year, kills more than 120,000
• common, preventable and treatable disease, that is characterized by airflow limitation that is not reversible. It is usually progressive and associated with an enhanced chronic inflammatory response in the airways and the lung to noxious particles or gases.

Question 5

WHOs definition of COPD:

Answer 5

“Chronic obstructive pulmonary disease (COPD), a common preventable and treatable disease, is characterized by persistent airflow limitation that is usually progressive and associated with an enhanced chronic inflammatory response in the airways and the lung to noxious particles or gases. Exacerbations and comorbidities contribute to the overall severity in individual patients.”

Question 6

Define Chronic Bronchitis:

Answer 6

chronic inflammatory condition of the small airways that results in a chronic productive cough; cough must last for three months in each of two successive years. Other causes of cough (bronchiectasis, malignancy, etc., must be ruled out).

Question 7

Define Emphysema:

Answer 7

defined by abnormal and permanent enlargement of the airspaces distal to the terminal bronchioles due chronic inflammation. There is destruction of the airspace walls but no overt fibrosis (like fibrosis caused by PNA). Emphysema can exist in individuals who do not have airflow obstruction, it is more common among patients who have moderate or severe airflow obstruction.

Question 8

Define Asthma:

Answer 8

a chronic inflammatory disorder of the airways and many cells and cellular elements play a role. The chronic inflammation is associated with airway responsiveness (bronchospasm) that leads to recurrent episodes of wheezing, breathlessness, chest tightness, and coughing. The airflow obstruction that occurs during these episodes is often reversible either spontaneously or with treatment.

Question 9

When is an asthma pt not considered to have COPD?

Answer 9

• Patients with asthma whose airflow obstruction is completely reversible are not considered to have COPD
• -Patients with asthma whose airflow obstruction does not remit completely are considered to have COPD

Question 10

Do Chronic bronchitis and emphysema commonly occur together?

Answer 10

yes

Question 11

Asthmatic Bronchitis:

Answer 11

terminology has not been officially endorsed in clinical practice guidelines
-Individuals with asthma may develop a chronic productive cough, either spontaneously or due to exposure (eg, cigarette smoke, allergen).

Question 12

COPD must have what?

Answer 12

• airflow obstruction
• Persons with chronic bronchitis, emphysema, or both are not considered to have COPD unless they have airflow obstruction

Question 13

Abnormalities of the airway in COPD:

Answer 13

include chronic inflammation, increased numbers of goblet cells, mucus gland hyperplasia, fibrosis, narrowing and reduction in the number of small airways, and airway collapse due to the loss of tethering caused by alveolar wall destruction in emphysema. Among patients with chronic bronchitis who have mucus hypersecretion, an increased number of goblet cells and enlarged submucosal glands are typically seen.

Question 14

COPD risk factors:

Answer 14

Suspected in patients with a history of smoking, occupational and environmental risk factors, or a personal or family history of chronic lung disease.

Question 15

How does COPD present?

Answer 15

Presents with progressive shortness of breath, cough, and sputum production, wheeze, including hemoptysis

Question 16

COPD Tx:

Answer 16

Treatment options include bronchodilators, inhaled corticosteroids, and systemic corticosteroids.
-Long-term oxygen therapy improves survival in severe COPD.

Question 17

COPD presentation and work up:

Answer 17

Most patients will present with mild to moderate disease
Severe disease cyanotic, tachypneic, on O2, peripheral edema, tachycardic
Complain of chronic cough, sputum production, dyspnea, SOB, possibly wheezing
Insidious onset, usually see in older people
These all get worse over time, so by age 60 you may see more complaints of more serious symptoms like SOB at rest, DOE, wheezing, chronic mucous production, breathlessness
History and physical exam, social history very important
Tobacco smoking is by far the main risk factor, it is responsible for 40% to 70% of COPD

Question 18

What do you test for in COPD Pts.?

Answer 18

Oxidative stress and an imbalance in proteinases and antiproteinases are also important factors in the pathogenesis of COPD, especially in patients with alpha-1 antitrypsin deficiency
If you have a patient with COPD or asthma with chronic airflow obstruction order a serum alpha-1 antitrypsin level to determine if they have this deficiency

Question 19

PE of COPD through out disease progression:

Answer 19

Early in the disease, the physical examination may be normal, or may show only prolonged expiration or wheezes on forced exhalation.
●As the severity of the airway obstruction increases, physical examination may reveal hyperinflation (eg, increased resonance to percussion), decreased breath sounds, wheezes, crackles at the lung bases, and/or distant heart sounds [55]. Features of severe disease include an increased anteroposterior diameter of the chest (“barrel-shaped” chest) and a depressed diaphragm with limited movement based on chest percussion.
●Patients with end-stage COPD may adopt positions that relieve dyspnea, such as leaning forward with arms outstretched and weight supported on the palms or elbows. This posture may be evident during the examination or may be suggested by the presence of callouses or swollen bursae on the extensor surfaces of forearms. Other physical examination findings include use of the accessory respiratory muscles of the neck and shoulder girdle, expiration through pursed lips, paradoxical retraction of the lower interspaces during inspiration (ie, Hoover’s sign) [56,57], cyanosis, asterixis due to severe hypercapnia, and an enlarged, tender liver due to right heart failure. Neck vein distention may also be observed because of increased intrathoracic pressure, especially during expiration.

Question 20

COPD testing:

Answer 20

No laboratory test is diagnostic for COPD, but certain tests are sometimes obtained to exclude other causes of dyspnea and comorbid diseases.
Anemia (CBC), heart failure (BNP).

Pulmonary function tests (PFTs), particularly spirometry, are the cornerstone of the diagnostic evaluation of patients with suspected COPD [60]. In addition, PFTs are used to determine the severity of the airflow limitation, assess the response to medications, and follow disease progression.

-CXR, SPO2, CBC, ECG

Arterial blood gas if showing moderate symptoms

Spirometry/PFTs is the first test for diagnosis of COPD and for monitoring disease progress.

Sleep study

Coughing up purulent, foul smelling phlegmAbx

If these fail, try a sputum culture

Advanced disease CT chest, exercise testing

All of the above should help you determine whether or not this is more chronic bronchitis versus emphysema

Question 21

Spirometry in COPD:

Answer 21

performed pre and post bronchodilator administration (eg, inhalation of albuterol 400 mcg) to determine whether airflow limitation is present and whether it is partially or fully reversible. Airflow limitation that is irreversible or only partially reversible with bronchodilator is the characteristic physiologic feature of COPD. Screening spirometry is not currently recommended.

-*The postbronchodilator ratio of FEV1/FVC determines whether airflow limitation is present. The postbronchodilator percent predicted value for FEV1 determines the severity (GOLDs severity) of airflow limitation.

Question 22

Spirometry and the difference between COPD and emphysema:

Answer 22

The differences between emphysema and COPD (without knowing the pathology) requires more information

FEV1 is decreased in both

Diffusion capacity of CO (DLCO) is decreased in emphysema and normal in COPD

CT is definitive test to determine presence of emphysema in living patient

Question 23

Tx of COPD:

Answer 23

• prevent/control symptoms
• reduce # of exacerbations
• improve respiratory capacity for increased exercise tolerance
• reduce mortality
• ongoing monitoring

Question 24

only 3 therapies to change natural history of COPD:

Answer 24

• stop smoking
• oxygen therapy
• lung volume reduction surgery

Question 25

COPD prevention:

Answer 25

STOP SMOKING!!!
Reduce environmental risk factors/occupational exposures
Pulmonary rehab physical training/exercise, disease education, nutritional, psychological and behavioral intervention.
Yearly spirometry
Vaccinations Influenza and Pneumococcal vaccines
Pharmacotherapy

Question 26

COPD tx for group A pts.:

Answer 26

-Short acting bronchodilators
-Short-acting beta agonists:
albuterol inhaled: (90 micrograms/dose inhaler) 90-180 micrograms (1-2 puffs) every 4-6 hours when required
levalbuterol inhaled: (45 micrograms/dose inhaler) 45-90 micrograms (1-2 puffs) every 4-6 hours when required
ipratropium bromide inhaled: (17 micrograms/dose inhaler) 34 micrograms (2 puffs) up to four times a day when required, maximum 204 micrograms/day
ipratropium bromide/albuterol inhaled: (18/103 micrograms/dose inhaler) 36/206 micrograms (2 puffs) every 6 hours when required

Question 27

Tx COPD group B pts:

Answer 27

short and long acting bronchodilators
-ADD Long-acting beta agonists:
salmeterol inhaled: (50 micrograms/dose inhaler) 50 micrograms (1 puff) twice daily or
formoterol inhaled: (12 micrograms/dose inhaler) 12 micrograms (1 puff) twice daily or
indacaterol inhaled: (75 microgram/capsule inhaler) 75 micrograms (1 capsule) once daily or
arformoterol inhaled: 15-30 micrograms nebulized twice daily

Question 28

TX COPD group C pts:

Answer 28

-same as B but add inhaled corticosteroid
-ADD inhaled corticosteroid:
beclomethasone dipropionate inhaled: (40 or 80 micrograms/dose inhaler) 80-240 micrograms/day given in 2 divided doses
budesonide inhaled: (90, 100, 180, 200, or 400 micrograms/dose inhaler) 180-600 micrograms/day given in 2 divided doses
flunisolide inhaled: (250 micrograms/dose inhaler) 500-1000 micrograms/day given in 2 divided doses
fluticasone propionate inhaled: (44, 110, 220 micrograms/dose inhaler) 88-440 micrograms/day given in 2 divided doses
-Also consider:
Combination long-acting beta-agonist and corticosteroid (single administration)
A phosphopiesterase inhibitor roflumilast: 500 micrograms orally once daily
theophylline: 300 mg/day orally (immediate-release) initially given in divided doses every 6-8 hours, increase to 400 mg/day after 3 days, then 600 mg/day after another 3 days; adjust dose according to serum drug level and response

Question 29

Tx COPD group D pts:

Answer 29

long-term oxygen therapy should be added to inhaled therapies, and possible surgical interventions should be considered.

Question 30

When is oxygen therapy used?

Answer 30

is instituted when the resting SPO2 is 88% or less, or 90% if there is evidence of right heart failure.

Question 31

Surgeries indicated for COPD?

Answer 31

Bullectomy for emphysema
Resection of large bullae compressing normal lung
Lung volume reduction surgery
Pneumonectomy of nonuniform emphysematous lung
Double lung transplantation
Can be life-saving, but is costly, can be lack of donor availability and requires lifelong immunosuppression

Question 32

COPD clinical goals:

Answer 32

-stop disease progression, keep exacerbations to a minimum, keep SPO2 at least 90-90%

Question 33

Whats an exacerbation?

Answer 33

Typically manifest as increased sputum production, more purulent sputum and worsening of dyspnea.
Although infectious etiologies account for most exacerbations, exposure to allergens, pollutants or inhaled irritants may also play a role.

Question 34

Bacterial infection is a factor in 70 to 75 percent of exacerbations, with up to 60 percent caused by:

Answer 34

Streptococcus pneumoniae
Haemophilus influenzae
Moraxella catarrhalis

Question 35

Antibiotic therapy has a small but important effect on clinical recovery and outcome.

Answer 35

Respiratory fluoroquinolone (Levofloxacin, Moxifloxacin)
Ceftriaxone + azithromycin

Question 36

Short courses of systemic corticosteroids may provide important benefits in patients with exacerbations of COPD

Answer 36

prednisone : 30-60 mg orally once daily for 5 days
methylprednisolone : 40-60 mg/day orally given once daily or in 2 divided doses for 5-7 days
Oxygen therapy to keep saturation Between 90-93%

Question 37

Asthma Highlights :

Answer 37

Patients present with recurrent episodes of shortness of breath, chest tightness, wheezing, or coughing.

Examination typically demonstrates an expiratory wheeze; however, in severe asthma there is poor air entry and the chest is silent.

Treatment is stepwise, based on symptoms. Patients need to monitor their peak expiratory flow daily and to be aware of the warning signs of a severe attack.

Some patients may develop progressive, irreversible obstructive lung disease.

Question 38

Asthma pathophys:

Answer 38

inflammation and airway hyperresponsiveness

Question 39

Asthma presentation and workup:

Answer 39

Complaints of recurrent episodes of dyspnea, chest tightness, wheezing, or coughing typically occur

History and physical, as always, timing of the symptoms

“Attacks” often have “triggers,” exposure to irritants such as tobacco smoke or fumes from chemicals, such as bleach; exercise, animals or seasonal fluctuations

More severely asthmatic people have night-time symptoms, waking them up from sleep

The exam may be normal in patients with bronchial asthma; chest auscultation may reveal expiratory wheezes.

With more severe asthma, the wheezes may be audible without the use of a stethoscope. In patients with severe exacerbations, the lung examination may be silent.

Question 40

Asthma testing:

Answer 40

CBC, CXR, SPO2

Spirometry!!! The diagnosis of asthma is confirmed by demonstrating reversibility of airflow obstruction (usually defined as improvement in FEV1 by 12% and 200 mL) to short-acting bronchodilator.

Question 41

Asthma testing:

Answer 41

CBC, CXR, SPO2

Spirometry!!! The diagnosis of asthma is confirmed by demonstrating reversibility of airflow obstruction (usually defined as improvement in FEV1 by 12% and 200 mL) to short-acting bronchodilator.
-Peak expiratory flow rate (PEFR) monitoring demonstrating diurnal variability (defined as [highest daily PEFR - lowest daily PEFR]/[highest daily PEFR]) can help diagnose asthma.

The diagnosis of asthma is supported if PEFR varies by at least 20% for 3 days in a week over several weeks, or PEFR increases by at least 20% in response to asthma treatment.

Question 42

Mild intermittent asthma:

Answer 42

Symptoms ≤2 times a week
Asymptomatic and normal peak expiratory flow (PEFR) between attacks
Attacks are brief with varying intensity
Nighttime symptoms ≤2 times a month
Forced expiratory flow at 1 second (FEV1) or PEFR ≥80% of predicted
PEFR variability <20%.

Question 43

Mild persistent asthma:

Answer 43

Symptoms >2 times a week but <1 time a day
Exacerbations may affect activity
Nighttime symptoms >2 times a month
FEV1 ≥80% of predicted
PEFR variability between 20% and 30%.

Question 44

Moderate persistent asthma:

Answer 44

Daily symptoms (but not nightly)
Use of short-acting beta agonists daily
Attacks affect activity
Exacerbations ≥2 times a week and may last for days
Nighttime symptoms >1 time a week
FEV1 >60% to <80% of predicted
PEFR variability >30%.

Question 45

Severe persistant asthma:

Answer 45

Continual symptoms
Limited physical activity
Frequent exacerbations
Frequent nighttime symptoms
FEV1 ≤60% of predicted
PEFR variability >60%.

Question 46

General overview of asthma TX:

Answer 46

Goal of treatment is to achieve maximum control of symptoms with the fewest medications

Guidelines recommend asthma severity and control be viewed as a ladder in which medication can be stepped up or stepped down based on the severity of the disease and adequacy of the control.

Regular assessment of patient’s asthma control should be carried out with the aim of stepping down the ladder if disease has been well controlled for at least 3 months.

All patients at all steps of therapy should receive adequate patient education and should take environmental control measures

Question 47

Acute Bronchitis highlights:

Answer 47

Acute illness with cough in a patient without underlying respiratory problems; usually caused by a viral infection transient condition

Main symptom is persistent cough, can take weeks to resolve

Cough is typically worse at night or with exercise; lasts >2 weeks in 50% and 4 weeks in 25% of patients; with or without bronchospasm and/or excessive mucus production.

Treatment is aimed at symptom reduction until infection is resolved and bronchial damage repaired.

Complications are rare; the primary complication is a post-bronchitis syndrome, which can produce a cough lasting several months.

Question 48

Epi of acute bronchitis:

Answer 48

In an ambulatory setting, cough is the most frequent reason for patients to seek care outside of a general medical examination.

Almost 5% of the general population develops acute bronchitis annually in the US

The highest incidence during the fall and winter months.

Although found in all age groups, acute bronchitis is most frequently diagnosed in children younger than 5 years, whereas chronic bronchitis is more prevalent in people older than 50 years.

Question 49

acute bronchitis etiology/pathophys:

Answer 49

Most cases of acute bronchitis are viral infections most common viruses include coronavirus, rhinovirus, respiratory syncytial virus, and adenovirus (same as URIs).

Bronchitis refers specifically to infections causing inflammation in the bronchial airways lower respiratory tract infection

The symptoms are due to acute inflammation of the bronchial wall, which causes increased mucus production along with edema of the bronchus.

Infection may clear in several days but repair of the bronchial wall may take several weeks Coughing

Question 50

Acute bronchitis presentation and workup:

Answer 50

COUGH!!! Productive cough < 30 days, Low grade fever, wheezes and/or rhonchi.

Cough should have been associated with recent/resolving URI, runny nose, sore throat, etc.

The diagnosis is primarily clinical, if you get tests, they are performed to rule out other causes of symptoms.

NO CXR, no labs, no sputum culture

CXR should be negative if truly acute bronchitis

Rule out chronic disease, PNA, asthma, etc.

Pulmonary function studies of patients with acute bronchitis demonstrate bronchial obstruction similar to that in asthma.

Question 51

Acute Bronchitis Tx:

Answer 51

For many patients with minimal cough that disrupts neither daily activity nor sleep, the best approach may be to offer no treatment.

For patients with significant symptoms who desire treatment, medications to reduce symptoms include expectorants and/or cough suppressants

Supportive care analgesics, antipyretics, antitussives, expectorant, hydration, rest

Significant wheezing, nocturnal cough, cough when they are physically active consider short-acting beta-agonist (albuterol) and/or antitussives

Question 52

Bronchiectasis highlights:

Answer 52

Patients often present with recurrent pulmonary infections, including a chronic daily productive cough with mucopurulent sputum production.

A sputum sample should be obtained when the patient is in a stable state and during acute exacerbations. Systemic antibiotics directed toward prior culture results should be administered.

Daily airway clearance is essential for treatment success.

Maintenance aerosolized antibiotics should be used for treatment of severe bronchiectasis or recurrent Pseudomonas aeruginosa infections.

Surgical therapy, including lung transplantation, should be considered for patients who continue to deteriorate despite optimal medical management.

Question 53

Bronchiectasis definition:

Answer 53

Bronchiectasis is the permanent dilation of bronchi due to the destruction of the elastic and muscular components of the bronchial wall.

It is often caused as a consequence of recurrent and/or severe infections secondary to an underlying disorder.

The majority of patients will present with a chronic cough and sputum production.

Question 54

Bronchiectasis epidemiology:

Answer 54

The prevalence worldwide is unknown due to the lack of standardized medical care and poor health care access in underdeveloped countries.

In the US, an estimated 110,000 individuals are affected, but data suggest that prevalence is increasing.

Bronchiectasis is more common with advancing age, ranging from 4.2 per 100,000 people ages 18 to 34 years to 272 per 100,000 people over 75 years old

However, the cause of bronchiectasis may not be identified, and hence the condition is often considered to be idiopathic. Congenital disorders and immune dysregulation (autoimmune or immune deficiency) may also cause bronchiectasis.

If affects women more commonly than men

Question 55

Development of bronchiectasis usually requires two things:

Answer 55

An infectious insult

Impaired drainage, airway obstruction, or a defect in host defense

Question 56

Post-infectious bronchiectasis:

Answer 56

Prior childhood respiratory infections due to viruses (i.e., measles, influenza, pertussis)
Prior infections with Mycobacteria or severe bacterial pneumonia
Exaggerated response to inhaled Aspergillus fumigatus image
Swyer-James or Macleod syndrome (a chronic manifestation of bronchiolitis or pneumonitis in childhood, characterized by unilateral pulmonary hypoplasia and radiographic hyperlucency).

Question 57

Immunodeficiency bronchiectasis:

Answer 57

Immune globulin deficiency

HIV infection

Question 58

Genetic bronchiectasis:

Answer 58

Cystic fibrosis
Ciliary dyskinesia or immotile cilia syndrome with or without Kartagener syndrome (an autosomal-recessive condition characterized by the triad of ciliary dyskinesia, situs inversus, and chronic sinusitis image
Alpha-1-antitrypsin deficiency

Question 59

Connective tissue disorders that cause bronchiectasis:

Answer 59

Rheumatoid arthritis

Sjogren syndrome.

Question 60

inflammatory bowel diseases that cause bronchiectasis:

Answer 60

Ulcerative colitis

Crohn disease.

Question 61

Bronchiectasis presentation/workup:

Answer 61

Presentation and Workup:

Persistent productive cough, daily mucopurulent sputum, fatigue, rhinosinusitis, dyspnea

History and Physical exam previous infections?

Crackles, high-pitched inspiratory squeaks, rhonchi, wheezing

CXR, SPO2, CBC, sputum cultures

PFTs and CT chest; CT is test of choice

Sweat chloride test (to role out cystic fibrosis) and alpha-1 antitrypsin test, serum immune globulins, rheumatoid factors, HIV test, aspergillus fumigatus skin prick test

Question 62

Bronchiectasis Tx:

Answer 62

Improved nutrition and exercise/physical therapy
Respiratory therapy airway clearance therapy
Nebulized bronchodilator
Nebulized hypertonic saline
Long term oral antibiotics macrolide, low dose daily or higher dose weekly
Suspected or high risk for Pseudomonas infection Inhaled antibiotic options include tobramycin, colistin, and gentamicin (every other month tx)
Acute exacerbation/mild disease full course abx
Acute exacerbation/advanced disease IV abx
Advancing disease surgery, lung transplant, mechanical ventilation

Question 63

Alpha-1 Antitrypsin deficiency highlights:

Answer 63

*Genetic disorder with an autosomal inheritance pattern and *codominant expression of alleles.

Pulmonary and hepatic manifestations include emphysema and cirrhosis.

Wegener granulomatosis and necrotizing panniculitis are infrequent complications but can prompt diagnosis.

Plasma AAT levels, protein phenotyping, and protein genotyping may be necessary for diagnosis.

Intravenous AAT augmentation therapy benefits some patients.

Question 64

Alpha-1 antitrypsin deficiency presentation and workup:

Answer 64

Presenting symptoms of pulmonary manifestations may include shortness of breath, shortness of breath on exertion, fatigue, wheezing, cough, and/or chest tightness.

May hear wheezing, see barrel chest on exam

Presenting symptoms of hepatic manifestations may include yellowing of the skin, fatigue, bleeding, bruising, abdominal distention, abdominal pain, and/or confusion.

The mean age at which smokers with AAT deficiency typically present with symptomatic pulmonary disease is 32 to 41 years.

CXR, CBC, AAT, CMP (LFTs), SPO2, PFTs reduced FEV1

Chest CT where the bronchiectasis and/or emphysema is localized; panacinar emphysema usually seen lower lobes

Question 65

Serum AAT levels should be measured when there is increased suspicion of disease:

Answer 65

early-onset emphysema
emphysema without recognizable risk factors
emphysema with basilar prominence
unexplained liver disease
necrotizing panniculitis
c-ANCA-positive vasculitis
family history of AAT deficiency
and/or unexplained bronchiectasis

Question 66

AAT deficiency Tx:

Answer 66

All patients with AAT deficiency should stop smoking and avoid pollution to help protect against respiratory manifestations. There is evidence demonstrating the rate of FEV1 decline to be worse in smokers compared with nonsmokers; however, no significant difference is demonstrated between ex-smokers and nonsmokers.

All patients with AAT deficiency also require hepatitis A and hepatitis B vaccination.

AAT deficiency manifestations are treated as per the usual treatments for COPD and/or liver disease.

Patients with airflow obstruction and low plasma AAT levels may benefit from intravenous AAT (also known as alpha-1 proteinase inhibitor) augmentation therapy alpha1-proteinase inhibitor: 60 mg/kg by intravenous infusion once weekly

Question 67

AAT augmentation Therapy:

Answer 67

AAT is produced in physiologic quantities in the liver and is then received in the lungs through hematologic circulation.
The process of intravenous AAT replacement therapy utilizes the same mode of delivery in order to provide the lungs with adequate levels of AAT to balance pulmonary physiologic and pathologic protease processes.
Research shows that weekly infusions of purified AAT from pooled human plasma are sufficient for increasing AAT in lung fluid and for protective levels of plasma AAT.

Question 68

AAT advancing/severe disease Tx:

Answer 68

Lung transplant
Manage liver disease/liver transplant
Avoid alcohol and pulmonary irritants