Module 3: Obstructive Pulmonary Diseases Flashcards
Bronchiectasis Etiology/Pathophysiology
Permanent, abnormal dilation of medium-sized bronchi due to inflammatory changes
* Destruction of elastic and muscular structures of the bronchial wall
* Cyclical process of inflammation results in damage which results in remodeling
* Colonization of microorganisms (Pseudomonas) results in weakening of walls and pockets of infection
Bronchial wall injury
Damages mucociliary mechanism, allows accumulation of mucus and bacteria within the pockets
Bacteria attract neutrophils which increases inflammation and causes edema
Impaired clearance of mucus by cilia leads to stasis of thick mucus
Reduced mucus clearance and decreased expiratory flow result
Bronchiectasis Causes/Risk Factors
Causes
No known cause in around 40% of cases
CF in children
Bacterial lung infections in adults
* Can follow 1 episode of severe pneumonia or from untreated, inadequately treated or pneumonia treatment that was delayed
Risk factors
Airway obstruction from mucus plugs, impaired pulmonary defenses, repeated aspiration
Some systemic problems
Bronchiectasis Clinical Manifestations
Cough with consistent production of thick, tenacious, purulent sputum
Hemoptysis can be severe, life-threatening
Pleuritic chest pain
Dyspnea
Clubbing
Weight loss
Anemia
Adventitious breath sounds, including wheezing
Bronchiectasis Complications
Pulmonary hypertension
Repeated exacerbations, often with chronic inflammation and hypoxemia
Colonization with multi-drug resistant organisms
Neovascularization (development of new blood vessels after injury) of bronchial arteries can lead to hemoptysis and hemorrhage
Bronchiectasis Diagnostic Studies
CT scan – gold standard
Chest x-rays – nonspecific abnormalities
Spirometry – obstructive pattern
Decreases in FEV1 and FEV1/FVC
**Decreases in Forced Expiratory Volume in the first second (FEV1) and the ratio of FEV1 to Forced Vital Capacity (FVC), denoted as FEV1/FVC, are significant findings in pulmonary function tests (PFTs)
FEV1 (Forced Expiratory Volume in the first second)
Definition: FEV1 is the volume of air that can be forcibly exhaled from the lungs in the first second of a forced expiratory maneuver, starting from full lung inflation. It reflects the ability of the airways to conduct air quickly out of the lungs.
Interpretation: A decrease in FEV1 indicates an obstruction to airflow. The severity of airflow obstruction can be graded based on the percentage of the predicted FEV1 value for a person of similar age, sex, height, and ethnicity.
FVC (Forced Vital Capacity)
Definition: FVC is the total volume of air that can be forcibly exhaled from the lungs after taking the deepest breath possible. It reflects the overall capacity of the lungs.
Interpretation: In obstructive lung diseases, FVC can be normal or slightly reduced due to early airway collapse during forced expiration, trapping air in the lungs.
FEV1/FVC Ratio
Definition: The FEV1/FVC ratio is a calculated ratio used in the diagnosis of obstructive and restrictive lung diseases. It represents the proportion of the lung capacity that can be expelled in the first second of forced exhalation.
Interpretation: A reduced FEV1/FVC ratio (typically less than 70%) is indicative of obstructive lung disease, suggesting that a significant proportion of the lung’s capacity cannot be quickly expelled. In contrast, in restrictive lung diseases, both FEV1 and FVC are reduced proportionally, maintaining a normal FEV1/FVC ratio.
Sputum cultures – confirm infection
CBC
AAT - An AAT study typically refers to the testing for Alpha-1 Antitrypsin (AAT) deficiency, a genetic condition that can lead to lung and liver disease. Alpha-1 Antitrypsin is a protein produced by the liver, which plays a critical role in protecting the lungs from inflammation caused by infection and inhaled irritants such as tobacco smoke. A deficiency in AAT can lead to chronic obstructive pulmonary disease (COPD), including emphysema, and liver disease, even in individuals who have never smoked.
Bronchiectasis Care
*Typically managed outpatient and to prevent flare ups
**treatment regimens often include antibiotics, bronchodilators, and corticosteroids. The choice of medication, route of administration, and duration of treatment depend on the specific diagnosis, severity of symptoms, and individual patient factors
*Antibiotics, type based on cultures
Bronchodilators
Types:
Short-Acting Beta-Agonists (SABA): Provide quick relief from acute bronchospasm and are used on an as-needed basis for symptoms.
Long-Acting Beta-Agonists (LABA): Used for long-term control of bronchospasm and to prevent symptoms, especially in asthma and COPD.
Anticholinergics: Block the action of acetylcholine, a neurotransmitter that causes bronchoconstriction. Used for both acute relief (short-acting forms) and long-term control (long-acting forms) of symptoms.
Purpose: Bronchodilators are used to relax bronchial muscles, thereby widening the airways and making breathing easier. They are a mainstay in the treatment of conditions like asthma and COPD.
Corticosteroids
Usage: Corticosteroids, both inhaled and systemic, are used to reduce inflammation in the airways, improve breathing, and prevent exacerbations of chronic lung diseases like asthma and COPD.
Inhaled Corticosteroids (ICS): Used regularly to control chronic inflammation and prevent exacerbations in asthma and COPD.
Systemic Corticosteroids: Used for short courses to treat acute exacerbations of asthma and COPD, or other inflammatory lung conditions.
Cystic Fibrosis (CF)
Inherited, autosomal recessive genetic disorder with altered transport of sodium and chloride ions in and out of epithelial cells
Airway obstruction due to changes in exocrine glandular secretions resulting in increased mucus production
**Primarily affects
Lungs
GI system - Pancreas and biliary tract
Reproductive organs
Incidence
About 30,000 people living with CF in US
More than 50% are adults
Median age at diagnosis is 6-8 months of age
2/3 of patients are diagnosed in the 1st year of life
Some not diagnosed until adulthood
Severity and progression varies
Prognosis has improved with early diagnosis, new therapies
Median predicted survival has increased to >46 years
Was 16 years of age back in 1970
CF Genetic Link
Autosomal recessive disorder found on chromosome 7
Makes a protein called CF transmembrane conductance regulator (CFTR)
* Mutations change the normal functions of the protein
* Channels in and out of epithelial cells are blocked
* Causes cells that line the passageways of lungs, pancreas, intestines, other organs to make secretions low in sodium chloride/water content
* Makes them abnormally thick and sticky
Plugs ducts in the organs causing scarring and resulting in organ failure
CF Pathophysiology
Cystic fibrosis (CF) is a genetic disorder that affects the exocrine glands, leading to the production of thick, sticky mucus that can cause a range of complications, especially in the respiratory and digestive systems.
Defective Chloride Secretion and Sodium Absorption
CFTR Protein Dysfunction: CF is caused by mutations in the gene that encodes the cystic fibrosis transmembrane conductance regulator (CFTR) protein. This protein functions as a channel on the surface of cells that controls the movement of chloride ions in and out of cells. In CF, defective CFTR protein leads to impaired chloride secretion into the airway lumen and increased sodium absorption back into the cells.
Mucus Dehydration: The abnormal ion transport results in decreased water content in the airway surface liquid, leading to the production of thick, dehydrated mucus.
Mucus Accumulation in the Airways
Tenacious Mucus: The dehydrated and sticky mucus cannot be easily cleared from the airways. It accumulates, obstructing the airways and creating an environment conducive to chronic bacterial infections and inflammation.
Ciliary Dysfunction: The thick mucus also impairs the function of cilia, the tiny hair-like structures that line the respiratory tract and help move mucus out of the airways. As a result, the clearance of mucus and pathogens is significantly reduced.
Airway Obstruction and Infection
Bronchiole Obstruction: The buildup of thick mucus leads to obstruction of the small airways (bronchioles), causing difficulty in breathing and decreased airflow.
Chronic Infection and Inflammation: The mucus provides a breeding ground for bacteria, leading to recurrent and chronic respiratory infections. The body’s response to these infections causes inflammation and further damages the airway walls.
Lung Tissue Destruction
Structural Changes: Chronic infection and inflammation lead to structural changes in the airways, including bronchiectasis (permanent enlargement of parts of the airways), scarring, and the development of fibrosis (thickening and scarring of connective tissue).
Air Trapping and Hyperinflation: Obstruction in the airways can also lead to air trapping, where air becomes trapped in the alveoli beyond the obstructed airways, causing hyperinflation of the lungs and further impairing respiratory function.
Progression of Respiratory Disease in CF
The respiratory manifestations of CF typically progress over time from affecting the small airways to involving the larger airways, with cumulative damage leading to significant respiratory morbidity and reduced lung function. Management strategies in CF focus on improving airway clearance, controlling infections, reducing inflammation, and addressing nutritional and gastrointestinal complications to improve quality of life and survival in individuals with CF.
Airway Infections in CF
Persistent, chronic, incurable airway infections, often seen in conditions like cystic fibrosis (CF) or chronic obstructive pulmonary disease (COPD), pose significant challenges in respiratory medicine. These infections lead to progressive lung damage and a host of complications:
Common Organisms
Pseudomonas aeruginosa: This bacterium is one of the most common pathogens involved in chronic lung infections, especially in individuals with CF. It is known for its ability to form biofilms, making it particularly difficult to eradicate and leading to chronic colonization of the airways.
Antibiotic Resistance
Repeated Exposures: Frequent and prolonged use of antibiotics to treat recurrent respiratory infections can lead to the development of antibiotic-resistant strains of bacteria. This makes subsequent infections harder to treat and can limit therapeutic options.
Inflammatory Response
Mediators of Inflammation: The body’s response to chronic infection involves the release of various inflammatory mediators, which contribute to the progression of lung damage. This ongoing inflammation exacerbates the cycle of infection and tissue destruction.
Disease Progression
Chronic Bronchiolitis and Bronchiectasis: The initial stages of lung damage involve inflammation and infection of the small airways (bronchiolitis) and the progressive dilation and destruction of the bronchial walls (bronchiectasis). These changes impair mucus clearance and create an environment conducive to further infections.
Pulmonary Vascular Remodeling: Chronic hypoxia (low oxygen levels) and inflammation in the lung tissue can lead to vascular remodeling, where the blood vessels in the lungs thicken and narrow. This is partly due to hypoxia-induced vasoconstriction, an adaptive response to redirect blood flow to better-oxygenated areas of the lung.
Pulmonary Hypertension and Cor Pulmonale
Pulmonary Hypertension (PH): The changes in pulmonary vasculature increase the resistance to blood flow through the lungs, leading to pulmonary hypertension. PH places additional strain on the right side of the heart, as it has to work harder to pump blood through the narrowed pulmonary arteries.
Cor Pulmonale: Over time, the increased workload on the right heart can lead to right ventricular hypertrophy (enlargement) and eventually right heart failure, a condition known as cor pulmonale. Symptoms of cor pulmonale include shortness of breath, swelling in the legs and abdomen, and fatigue.
CF - More Complications - Blebs/Large Cysts
Blebs and large cysts in the lungs represent significant structural changes and are indicative of underlying lung damage. These abnormalities can occur in various pulmonary conditions, including chronic obstructive pulmonary disease (COPD), cystic fibrosis (CF), and pneumoconiosis, or they can be idiopathic in nature. The presence of blebs and cysts signifies severe emphysematous changes or fibrocystic processes within the lung tissue, leading to the destruction of alveolar walls and the formation of large air-filled spaces.
Complications
Pneumothorax:
Description: A pneumothorax occurs when air escapes from the lung into the space between the lung and the chest wall (pleural space), causing the lung to collapse. Blebs and cysts are weak spots on the lung surface that can rupture, releasing air into the pleural space.
Consequences: Depending on the size of the pneumothorax and the underlying lung health, symptoms can range from mild discomfort to severe respiratory distress and hypoxemia. A tension pneumothorax, where air continues to enter the pleural space without a way to escape, is a medical emergency requiring immediate intervention.
Hemoptysis:
Description: Hemoptysis, or coughing up blood, can occur when fragile blood vessels within or adjacent to the blebs or cysts rupture. The severity of hemoptysis can vary from small streaks of blood to life-threatening bleeding.
Consequences: Significant hemoptysis can compromise the airway, reduce oxygenation, and in severe cases, lead to asphyxiation. The presence of blood in the airways can also predispose to infection and further complicate the clinical picture.
CF Complication - Pancreatic Insufficiency
Pancreatic insufficiency is caused by mucus plugs in
pancreatic ducts; results in atrophy and progressive fibrotic cyst formation
Exocrine function of pancreas is altered or may be lost
completely
Insufficient production of enzymes lipase, amylase, and proteases do not allow for absorption of nutrients
Malabsorption of fat, protein, and fat-soluble vitamins
manifest as
Steatorrhea
* Large, oily, frequent bowel movements
Failure to grow and gain weight
* Low body mass index (BMI)
Osteopenia and osteoporosis
* Related to malnutrition, malabsorption of vitamin D, low testosterone levels, chronic infections
Pancreatitis may occur
Pancreatic insufficiency management
Replace pancreatic enzymes and supplements
Adequate fat, calorie, vitamins (A, D, E, K)
Caloric supplements
Added diet salt with increased sweating (hot weather, fever, intense physical activity)
Insulin if hyperglycemia develops
CF Diabetes
CF-related diabetes (CFRD) is related to
underdevelopment of islet cells in utero and later
destruction of islet cells over the lifetime
Has both type 1 and type 2 characteristics
Make insulin too late to fully respond to carbohydrate intake
CF GI Problems
Many also have GI problems
GERD, gallstones, and cirrhosis
Mucus deposits damage liver and gallbladder
Portal hypertension
DIOS (distal intestinal obstruction syndrome)
* Thick, dehydrated stool and mucus cause intermittent
obstruction at ileocecal junction
* May appear to have small bowel obstruction
Partial or complete DIOS
Medical management
* Options: prokinetic agents, mucolytics, stimulant laxatives, lactulose, polyethylene glycol (PEG) electrolyte solution
* Careful monitoring of bowel habits and patterns
Surgery if medical not successful
* Prevent ischemic bowel
Signs of CF in Adults and Kids
Early manifestations that suggest CF
Meconium ileus in the newborn (20% of people)
*meconium is so thick and sticky that it cannot be passed through the intestines normally, causing a blockage.
Acute or persistent respiratory symptoms
Failure to thrive or malnutrition
Steatorrhea (large, oily, frequent BM)
Bronchiectasis
Family history
Atypical presentation in adults
Diabetes
Infertility
Commonly seen: frequent cough
* Becomes persistent
* Produces thick, purulent sputum
URI manifestations
* Chronic sinusitis, nasal polyposis
* Recurring lung infections – bronchiolitis, bronchitis, pneumonia
* Clubbing
Exacerbations increase in frequency
Increased cough and sputum
Weight loss
Decreased lung function
Eventually results in respiratory failure
DIOS
* Thick, dehydrated stool and mucus cause intermittent
obstruction at ileocecal junction
RLQ pain, nausea, vomiting, palpable mass
Thin, low BMI
Frequent, bulky, foul-smelling stools
Delayed puberty
Females: menstrual irregularities, amenorrhea, difficulty conceiving; most are able to conceive/have viable infants
Males: vas deferens doesn’t develop
* Do make sperm normally; able to father a child with assisted reproductive technology
CF Complications
CFRD
Bone disease
Sinus disease
Liver disease
Pneumothorax – rare but serious
Hemoptysis (rare but can be life-threatening if massive)
Liver failure and bowel obstruction in severe cases
Late complications caused by pulmonary hypertension
Respiratory failure
Cor pulmonale
CF Diagnostic Studies
Clinical presentation, family history, lab and genetic testing
Gold standard: *sweat chloride test with pilocarpine
iontophoresis method
Pilocarpine carried by electric current is used to stimulate sweat production (in both arms)
Sweat is collected and analyzed
Sweat chloride values >60 mmol/L are considered positive for CF
* Sweat glands secrete normal volumes of sweat but do not absorb sodium chloride as it moves through sweat duct
* Excrete 4 times normal amount of sodium and chloride in sweat
Genetic testing done is results from sweat chloride test are uncertain
Can send blood or cell sample to specialty lab
Most labs test for only the most common mutations of the CF gene
More than 1700 mutations cause CF; screening is difficult
Care for CF Patients
Management focuses on relieving airway obstruction and controlling infection
Aerosol and nebulizer treatments promote drainage of thick bronchial mucus; drugs
Dilate airways, liquify mucus, promote clearance
* Inhaled dornase alpha (Pulmozyme)
* Inhaled hypertonic saline (7%)
* Bronchodilators (e.g., β2-adrenergic agonists)
Airway clearance techniques (ACTs)
Loosen mucus
* CPT with postural drainage, percussion, vibration
* High-frequency chest wall oscillation systems
Specialized expiratory techniques use airflow to remove loosened secretions
* PEP devices (Positive Expiratory Pressure)
**PEP devices create resistance during exhalation, which helps maintain airway patency and increases the pressure in the airways. This pressure helps prevent airway collapse, facilitates the opening of obstructed or collapsed airways, and promotes the movement of mucus towards the larger airways where it can be more easily cleared.
* Breathing exercises
* Pursed-lip breathing
* Huff coughing
**Also known as a forced expiratory technique, huff coughing involves taking a breath in and then exhaling forcefully in a series of “huffs” from the mouth, like fogging up a mirror. It’s less forceful than a standard cough but is effective in moving mucus from the smaller to the larger airways.
CFTR genotyping done for all patients
Determines if they carry a mutation that is a target of CFTR modulator therapy
Ivacaftor (Kalydeco) and Ivacaftor/lumacaftor are used to treat patients with specific CFTR gene mutations
Most patients with CF die of complications from lung
infection
Early intervention with antibiotics
Choice of antibiotic based on sputum culture results
2 antibiotics with different mechanisms of action are usual treatment (10 days to 3 weeks or longer) or chronic suppression therapy
Drugs are abnormally metabolized and quickly excreted— may need prolonged high-dose therapy
Pseudomonas
Difficult to treat; organism forms a biofilm that protects it from antibiotics
Aerosolized tobramycin, twice a day, every day, every other month
Azithromycin used longer than 6 months decreases
exacerbation frequency; may have anti-inflammatory affects
Pneumothorax Care
Large Pneumothorax
Chest Tube Drainage: For a large pneumothorax, immediate intervention typically involves the insertion of a chest tube to evacuate the air from the pleural space, allowing the lung to re-expand. This procedure is performed under sterile conditions, often in an emergency or surgical setting.
Recurrent Pneumothorax
For patients experiencing recurrent pneumothoraces, more definitive treatments may be necessary to prevent future episodes:
Pleural Sclerosis: Involves the instillation of a sclerosing agent into the pleural space, causing the pleural layers to adhere to each other and eliminating the space where air could accumulate.
Mechanical Pleurodesis (Pleural Stripping or Abrasion): A surgical procedure where the pleural surfaces are mechanically abraded to induce scarring and adherence between the lung and chest wall, preventing recurrence of pneumothorax.
Massive Hemoptysis
Bronchial Artery Embolization: A minimally invasive procedure performed by interventional radiologists where the bleeding bronchial artery is identified via angiography and then occluded using embolic materials. This procedure can effectively control bleeding and is less invasive than surgical options.
Lung Transplant
For patients with end-stage lung diseases that are refractory to medical management, a lung transplant may be considered. This involves replacing one or both diseased lungs with healthy lungs from a deceased donor.
Interprofessional Care: Managing a lung transplant patient requires a coordinated effort from a team including pulmonologists, transplant surgeons, transplant coordinators, nurses, respiratory therapists, physiotherapists, pharmacists, and social workers, among others.
Interprofessional Care Considerations
Collaborative Decision-Making: Effective management of these complex conditions involves collaborative decision-making, taking into account the patient’s overall health, preferences, and the expertise of the multidisciplinary team.
Long-Term Management: Post-intervention care, especially for patients undergoing pleurodesis, embolization, or lung transplant, includes long-term monitoring for complications, pulmonary rehabilitation, and adherence to medication regimens.
Patient and Family Education: Educating the patient and family about the condition, treatment options, and self-care post-intervention is crucial for successful outcomes.
Asthma
Diverse disease characterized bronchial hyperreactivity
with reversible expiratory airflow limitation (spontaneously or with treatment)
Signs and symptoms may vary
* Minor asthma - mild SOB and chest tightness
* Major asthma attack – severe SOB, accessory muscle use, stridor, severe hypoxemia leading to respiratory and/or cardiac arrest if untreated
Clinical course is unpredictable
Asthma Gender Considerations
Men
Affects more boys before
puberty
Most likely to have less
severe symptoms by late
teen years
Women
Affects more women in
adulthood
Higher incidence and severity
among 40-60 years of age
More likely to need
hospitalization if come to ED
Higher overall mortality
URI as Asthma Trigger
Respiratory tract infections
Major trigger of acute asthma attacks
URIs decrease diameter of airways and induce airway
hyperresponsiveness
Contribute to altered respiratory function/worsen asthma
* Viral-induced epithelial cell changes
* Accumulation of cells that enhance inflammation
* Edema of airway walls
Risk Factors for Asthma
Atopy - genetic predisposition to develop an allergic
(immunoglobulin E [IgE]–mediated) response to common allergens
GERD more common in persons with asthma
Reflux may trigger bronchoconstriction as well as cause aspiration
Asthma medications may worsen GERD symptoms (beta2-agonists relax lower esophageal sphincter)
Treating GERD can
* Improve nocturnal asthma control
* Improve quality of life
* Prevent asthma symptoms
Drugs and food additives
Asthma triad: nasal polyps, asthma, sensitivity to aspirin and NSAIDs
* Wheezing develops in about 2 hours, also see profound rhinorrhea, congestion, tearing, and angioedema
Salicylic acid and NSAIDs—must avoid
* Found in many OTC drugs, foods, beverages, and flavorings
* Teach patients to read labels
* May improve with desensitization (daily administration of the drug under the care of an allergist)
Oral β-Adrenergic blockers, topical eye drops—can cause bronchospasm
ACE inhibitors—dry, hacking cough
Sulfite-containing preservatives
* Eyedrops, IV corticosteroids, inhaled bronchodilators
Tartrazine (yellow dye no.5) and sulfiting agents
* Common preservatives and sanitizing agents
* Fruits, beer, wine, and salad bars (prevent oxidation)
Food allergies triggering asthma reactions in adults are rare
Exercise Induced Asthma
Asthma that is induced or becomes worse during physical exertion
* Exercise-induced asthma (EIA) or exercise-induced
bronchospasm (EIB)
* Worse during activities in cold, dry air
Airway obstruction occurs with changes to mucosa from hyperventilation, inhaling cool or rewarmed air, airway edema
(from capillary leakage in airway wall)
* EIB often occurs after <10 minutes of vigorous exercise; resolves within 60 minutes
Occupation Induced Asthma
Occupational factors
Occupational asthma—most common job-related respiratory problem
Exposure to diverse irritating agents
* Include: wood dusts, laundry detergents, metal salts, chemicals, paints, solvents, and plastics
May take months or years of exposure
Arrive at work well, but experience a gradual decline by end of day
Psychological Asthma
Psychologic factors
Symptoms worsen with stress
Asthma attack can cause panic, stress, anxiety
* Lead to bronchoconstriction through stimulation of cholinergic reflex pathways
Extreme behavioral expressions (crying, laughing, anger, fear) can lead to hyperventilation and hypocapnia
Asthma Pathophysiology
Main pathophysiologic process is persistent and variable inflammation of airways
Exposure to allergens or irritants triggers the inflammatory cascade involving a variety of inflammatory cells
Inflammation leads to bronchoconstriction,
hyperresponsiveness, and edema of airways which means limited airflow
Asthma Early Response
Early-phase response
Occurs within minutes after exposure to an allergen or irritant
Generally resolves within 1-2 hours
Symptoms can recur 4-6 hours later due to influx of
inflammatory cells
* Symptoms repeat or are worse
Mast cells release inflammatory mediators when an allergen cross-links IgE receptors
* Mediators include leukotrienes, histamine, cytokines,
prostaglandins, and nitric oxide
Asthma Inflammatory Mediators Effect
Inflammatory mediators effect
Blood vessels—vasodilation and increased capillary
permeability (runny nose)
Nerve cells (itching)
Smooth muscle cells (bronchial spasms and narrowed
airway)
Goblet cells—mucus production
Edema of airway mucosa, muscle spasm, accumulation of secretions cause expiratory airflow obstruction
Asthma Step Therapy
Metered Dose Inhaler (MDI)
MDI—small, hand-held, pressurized devices
Deliver measured dose with activation; 1 to 2 puffs
Can be used with spacer or holding chamber to
* Reduce oropharyngeal medication deposition
* Increase delivery to lungs
* Reduce problems with hand-breath coordination
Teach patients to follow package inserts as MDIs vary
Dry Powdered Inhaler (DPI)
DPI (dry powder inhaler)
Simpler to use than MDIs
Powdered medication; breath activated
Advantages over MDIs:
* Less manual dexterity
* No need to coordinate device puffs with inhalation
Disadvantages:
* Low FEV1—inadequate inspiration
* Not all common meds available as DPI
* Powder may clump if exposed to humidity
COPD Pathophysiology
Characterized by chronic inflammation of airways, lung
parenchyma (functional tissue in an organ), and pulmonary blood vessels
Defining feature: airflow limitation not fully reversible during forced exhalation due to
Loss of elastic recoil
Airflow obstruction from mucous hypersecretion, mucosal edema, and bronchospasm
Disease progression marked by worsening
Abnormalities in airflow limitation
Air trapping
Gas exchange
Severe disease
Pulmonary hypertension
Systemic manifestations
Impaired or destroyed lung tissue exists alongside normal tissue
Main characteristic of COPD is the inability to expire air
Main site of airflow limitation is the smaller airways
* Peripheral airways are obstructed and trap air during expiration results in increased residual volume which results in barrel - shaped chest (respiratory muscles cannot function effectively)
* FRC is increased; passive expiration of air is difficult
* Patient becomes dyspneic and has limited exercise capacity as they try to inhale against overinflated lungs
COPD - Inflammation Process
Primary process is inflammation
Inhalation of noxious particles and gases results in
inflammation which results in damage to lung tissue and impaired normal defense mechanisms and repair processes
Predominate inflammatory cells are neutrophils,
macrophages, and lymphocytes
Oxidants contribute to structural destruction
As air trapping increases, alveolar walls are destroyed, resulting in formation of bullae and blebs
Bullae and blebs have no surrounding capillary bed resulting in ventilation-perfusion (V/Q) mismatch resulting in hypoxemia and hypercapnia (especially with severe disease and in late stages)
Excess mucus production
Increased number of mucus-secreting goblet cells
Enlarged submucosal glands
Cilia dysfunction
Stimulation from inflammatory mediators
Not all patients with COPD have sputum production
COPD is a systemic disease as a result of chronic
inflammation
Cardiovascular diseases are common
Other: osteoporosis, diabetes, metabolic syndrome
