Pulmonary Obstructive Flashcards
1
Q
What is COPD?
A
- A disease state characterized by the presence of airflow obstruction due to chronic bronchitis or emphysema
- Airflow obstruction is generally progressive
- may be accompanied by airway hyper-reactivity (bronchospasm)
-
NOT reversible in progressive COPD
- may be partially reversible-in asthma situation
2
Q
What is obstructie pulmonary disease?
A
- Airway obstruction that is worse with expiration –>resistance.
- Pt can inhale approp but cant exhale properly
- Common signs and symptoms
- Dyspnea (diff breathing)
- wheezing (in severe case can hear w/o steth)
- Common obstructive disorders
- Asthma, Emphysema, Chronic bronchitis
- Also bronchiectasis & CF
3
Q
What is asthma? S/S?
A
- Chronic inflammatory disorder of the airways
- Inflammation causes:
- Recurrent episodes of wheezing
- breathlessness
- chest tightness, and cough, particularly at night and in the early morning.
- Hyper-responsive to stimuli
- Usually associated with widespread but variable airflow obstruction that is often reversible (spontaneously or with Rx)
- Spontaneously - ie ppl w/ exercise induced asthma. Running & cold outside both exacerbates the asthma. If they stop exercising and come inside, it reverses & they’re more comfortable
4
Q
What is atopic asthma?
A
-
Atopic - the genetic predisposition for the development of an IgE-mediated response to common aeroallergens
- Strongest identifiable predisposing factor for developing asthma
- Pic of atopy: Genetic background + environmental factors that together lead to atopy →
- T cell regulation = more prevalent to TH2 cells instead of TH1 (which (TH1 are norm response against pathogens)
- → IgE mediated mast cell degranulation with release of platelet activating factor, leukotrienes, adhesion molecules → cell recruitment and inflammation
5
Q
What stimuli can provoke symptoms of asthma?
A
- Allergens
- Pharm agents: BB, ASA, NSAIDS, sulfiting agents
- Infections: respiratory viruses
- Exercise: follow exertion rather than after it
- Emotional stress: endorphins and vagal mediation
6
Q
Risk factors for asthma?
A
- Atopy
- Serum IGE increased
- Family hx of allergic diseases- genetic linkage between IGE and atopy
- Positive wheal and flare skin rxn to airborne allergens – allergist does test; how to dx ppl w/ asthma
7
Q
Diagnosis of asthma?
A
- Skin wheel tests?
- PFTs
- Diagnosis based on flow-volume curves
-
FEV 1and FEV1/FVC ratio decreased (bc FEV1 is dec)
- FEV1 – forced expiratory vol in 1 sec of expiratory phase
- FVC = forced vital capacity
- Ex: if FEV1 < 35% for predicted size (IBW)→ severe (status asthmaticus)
-
FEV 1and FEV1/FVC ratio decreased (bc FEV1 is dec)
- Diagnosis based on flow-volume curves
- Predicted = for Ideal Body Wt size (ibw)
- How we use flow vol curves to dx pts = this table
- In mild to mod asthma – the pao2 & paco2 tend to be still fairly Ok.
- Marked or severe → dramatic decrease in Pao2 & increase in PaCO2 that lead to other systemic probs
8
Q
Pathophysiology of Asthma?
A
- Allergen or irritant exposure results in a cascade of inflammatory events (IgE mediated) leading mast cell degranulation→ to acute and chronic airway dysfunction
- airway walls thicken due to allergen exposure cascade
- Mast cell degranulation (simultaneously causes 2 things to happen)
- → release of vasoactive mediators (vasodilation- increase in alveoli lung capillary permeability)
- → release of chemotactic mediators (neutrophils, eosinophils, lymphocytes)
* Autonomic dysregulation → increase in vasodilation and bronchospasm
* Release of toxic neuropeptides → epithelial squamous cell damage → fibrosis and airway obstruction
- → release of chemotactic mediators (neutrophils, eosinophils, lymphocytes)
- All of this together leads to (blue boxes)
If asthma attacks continue to occur & don’t get adequate or quick treatment →
- Results in bronchial hyperresponsiveness, airway obstruction, epithelial cell destruction and fibrosis
9
Q
COPD characteristics?
A
- Pathologic deterioration in elasticity or recoil-airway closure
- Can lead to airway closures -→ leading to atelectasis and concomitant w/ mucous release \
- Rigidity of bronchiolar wall
- → collapse of AW during exhalation
- Increase in gas velocity, lower pressure in bronchiole → a/w collapse (laminar turns into turbulent flow)
- d/t mucous plugs w/in proximal portions of lung (all this due to increased secretions)
- Increased secretions
- Exacerbates bronchospasm
- Over time, destruction of lung parenchyma-enlargement of air sacs, development of emphysema
10
Q
Risk Factors COPD?
A
-
*Cigarette smoking*
- 90-95% of COPD caused by smoking
- Passive smoking
- Second hand smoke if live w/ smoker
- Chronic infections of lung
- Ex: CF, Chronic bronchitis pts
- Occupational factors: w/o other factors
- Ex: coal mining, textile factories? Dentists?
-
Genetic-a1-antitrypsin deficiency
-
Only known genetic abnormality that leads to COPD
- Accounts for less than < 1% of cases
-
Alpha1AT helps to maintain the balance b/w the proteases & protein building blocks of lungs
- When imbalance w/ the deficiency → get breakdown of lung tissue by proteases → leads to COPD
-
Only known genetic abnormality that leads to COPD
11
Q
What is the mechanism of air trapping in COPD?
A
- Mucous plugs and narrowed airways cause air trapping and hyperinflation on expiration.
- During inspiration: the airways are pulled open
- Normal→ appropriately by the muscles that are still functioning, allowing gas to flow past the obstruction.
- During expiration: decreased elastic recoil of the bronchial walls AND mucous plugs → results in collapse of the airways (bronchial wall collapse) and prevents normal expiratory airflow
- Outpouching of alveolar walls overtime → increasing lung volumes that don’t take part in gas exchange.
- Exhaled volume already CO2 rich and O2 poor
- Outpouching of alveolar walls overtime → increasing lung volumes that don’t take part in gas exchange.
12
Q
Diagnosis of COPD?
A
- Chronic productive cough
- Airflow obstruction
- dx w/ flow vol loop
- Pulmonary function tests
- FEV1/FVC ratio decreased
-
Great decrease in FEF 25-75%
- Differential dx of obstructive vs restrictive lung dx = FEV1/FRC ratio
13
Q
What does the lung volume diagram look like in pt with COPD?
A
- In the presence of obstructive lung disease,
Increased
- Residual volume (RV) and functional residual capacity (FRC) are increased
- Total lung capacity (TLC) is normal to increased
- RV/TLC ratio is increased.
Reduced:
- Vital capacity (VC) is normal to decreased (during end of dx = dec)
- Small TV reduction
- ERV (expiratory reserve volume) – really reduced
- don’t tolerate apneic periods bc they don’t have a good reserve. They’ll need increase time pre-oxygenating & they start desatting quicker; IC, inspiratory capacity
- **Bigger isn’t better here bc the dilated lung tissue w/ loss of elastic recoil leads to worse gas exchange
14
Q
How do we grade the severity of COPD?
A
- Spirometric Classification
- Based on postbronchodilator FEV1 measurement
- Do baseline then give bronchodilator & assess on spirometric testing
- Mild COPD → > 80% of predicted FEV1
- Moderate: 50% < FEV1< 80% predicted
- Greater than 50% but less than 80% predicted
- Severe: 30% < FEV1 < 50% predicted
- Very severe: < 30% predicted or < 50% predicted plus changes in PaO2 or PCO2
- Needs vent assistance, o2 , & possible lung resection to remove areas of lungs that aren’t functioning properly to allow the areas that are functioning to improve in their fxn, and/or lung transplant last resort
- Based on postbronchodilator FEV1 measurement
- FEV1/FVC ratio is dec to < 70% of where we want it to be in every stage.
- So everyone w/ COPD has FEV1/FVC ratio reduction.
- How we diagnose them.
- Grade the severity look at FEV1 & eventually Pao2/Paco2
- So everyone w/ COPD has FEV1/FVC ratio reduction.
15
Q
What is chronic bronchitis
A
hallmark: purulent prod cough w/ lots of mucus= hallmark of CB
- Hypersecretion of mucus and chronic productive cough that lasts for at least 3 months of the year and for at least 2 consecutive years
- 2019 – develop cough, hypersx of mucous January to March
- 2020- 3 mo again where heavy mucous, cough
- 2 years in a row → chronic Bronchitis (usually get antibiotics)
- Inspired irritants increase mucus production and the size and number of mucous glands
-
The mucus is thicker than normal
- All this causes→ Ciliary damage (pt cant cough and expectorate it)
- Causes → Inflamed & narrowing of passages
- All this causes→ Ciliary damage (pt cant cough and expectorate it)
17
Q
Diff between “pure chronic bronchtis” and “pure emphysema” (although both are typically seen in COPD)
A
- Picture: Anatomic distribution of Pure chronic bronchitis and Pure emphysema.
- Typically smokers will have a combo of both
- Pure Chronic Bronchitis:
- Large Airways → inflammation, chronic bronchitis
- Small Airways → peribronchial fibrosis and airway obstruction (accumulation of mucous that causes ciliary damage)
- Pure Emphysema:
- Loss of elastic recoil and large airways impacted overtime.
18
Q
What is centriacinar emphysema? Panacinar emphysema?
A
- Diagram of normal structures within the Acinus (the fundamental unit of the lung).
- Terminal bronchiole (not shown) is immediately proximal to the respiratory bronchiole. & alv ducts & alveolus
- Centriacinar emphysema: dilation that initially affects the proximal respiratory bronchioles.
-
Panacinar emphysema: initial distention of the peripheral structures (i.e., the alveolus and alveolar duct);
- the disease later extends to affect the respiratory bronchioles.
In late stage emphysema see both types & whole acinus is impacted
* Acinus = gas exchange portion of the lungs
19
Q
How does tobacco lead to emphysema?
A
Smoke cigarette – inhale → reactive oxygen species and free radicle release
- IL-8, etc release → neutrophils activated and inactivation of antiproteases (alpha 1 antitrypsin)
- Just like → Genetic-a1-antitrypsin deficiency
-
-a1-antitrypsin = Antiprotease → prevents protein breakdown of lung involved in elastic recoil of lung and lung matrix
- Inactivation of antiprotease causes the breakdown of elastic structure in lung
- Functional A1AT deficiency- smokers
- Congenital A1AT deficiency - < 1 % pop
- Inactivation of antiprotease causes the breakdown of elastic structure in lung
- Actual tissue damage → battle b/t proteases and antiproteases leans more towards proteases (breakdown the walls)
- Causes increase in alveolar macrophages, elastase, and metallo-protinases
- Macrophages elastase start to breakdown elastin in lung and other tissues → emphysema
- The protease-antiprotease imbalance and oxidant-antioxidant imbalance are additive in their effects and contribute to tissue damage.
- α1-Antitrypsin (α1AT) deficiency can be either congenital or “functional” as a result of oxidative inactivation.
- * smokers have an increase in free radicals. They inactivate anti-proteases. (normally they prevent breakdown of proteins in lungs and tissues – block them=damage)
- Nicotine also a ROS?
20
Q
Pathogenesis of COPD (emphysema and chronic bronchitis)
A
Green box: tobacco smoke or airway pollution → inflammation of airway epithelium → infiltration of cytokines
→ systemic effects
→ inhibition of normal antiproteases
Leads to→ continual bronchial airway inflammation and irritation and increase protease activation with breakdown of elastin and CT of lung → chronic bronchitis and emphysema
All leads to blue box
- →* Cor pulmonale = heart dx caused by lung dx, generally involving the vasculature of the lungs bc of hypoxic pulm vasoconstriction→ which then leads to pulm htn which downstream has an effect on CV fxn
- hypoxemia leads to hypoxic pulm vasoconstriction… Pulm HTN with prolonged vasoconstriction and then leads to cor pulmonale
21
Q
Summary of all obstructive lung diseases?
A
- Normal
- Goblet cell- mucous prod
- Emphysema
- Some areas of normal alveoli and some alveoli without fibrosis but can see have disease
- Chronic bronchitis
- Increase in inflammation of epithelium
- Increase in mucous formation and accumulation of mucous plugs
- Hyperinflated alveoli not collapse prop with exirpation
- Bronchial asthma
- Degranulation of mast cell (IgE mediated resp to allergens in air)
- Some mucous
- Hyperinflation
Goblet cells=where muc formed
22
Q
What are pores of Kahn?
A
Little pores sitting between alveoli and allow the alveoli to communicate.
- When you take a breath in:
- If its shallow & there’s a mucous plug → the air may not enter all of the alveoli bc they’re plugged.
- The pores of Kohn are closed when taking shallower breath.
- If take a deep breath → you inspire air & hopefully open the pores, even if the alveoli have muc plugs in them, air can indirectly flow from alveoli without mucous plugs to alveoli w/ plugs
- Pores = secondary mechanism of getting airflow to alveoli that may have muc plugs
- If its shallow & there’s a mucous plug → the air may not enter all of the alveoli bc they’re plugged.
