Pulmonary Obstructive

Question 1

What is COPD?

Answer 1

• 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

Question 2

What is obstructie pulmonary disease?

Answer 2

• 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

Question 3

What is asthma? S/S?

Answer 3

• 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

Question 4

What is atopic asthma?

Answer 4

• 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

Question 5

What stimuli can provoke symptoms of asthma?

Answer 5

• Allergens
• Pharm agents: BB, ASA, NSAIDS, sulfiting agents
• Infections: respiratory viruses
• Exercise: follow exertion rather than after it
• Emotional stress: endorphins and vagal mediation

Question 6

Risk factors for asthma?

Answer 6

• 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

Question 7

Diagnosis of asthma?

Answer 7

• 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)
• 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

Question 8

Pathophysiology of Asthma?

Answer 8

• 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)
  
  • 1. → release of vasoactive mediators (vasodilation- increase in alveoli lung capillary permeability)
  • 2. → 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
• 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

Question 9

COPD characteristics?

Answer 9

• 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

Question 10

Risk Factors COPD?

Answer 10

• *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

Question 11

What is the mechanism of air trapping in COPD?

Answer 11

• 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

Question 12

Diagnosis of COPD?

Answer 12

• 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

Question 13

What does the lung volume diagram look like in pt with COPD?

Answer 13

• 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

Question 14

How do we grade the severity of COPD?

Answer 14

• 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
• 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

Question 15

What is chronic bronchitis

Answer 15

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

Question 16

What is emphysema?

Answer 16

Hallmark: SOB, cant catch breath bc hard time exhaling, so next inspiration after doesn’t help.

• Abnormal permanent (irreversible) enlargement of the gas-exchange airways accompanied by destruction of alveolar walls without obvious fibrosis (vs obvious fibrosis w/ CF)
• Loss of elastic recoil

2 Types of Emphesema:

• 1. Centriacinar emphysema (below) – central portion of acina involved – resp bronchioles
• 2. Panacinar emphysema (below) – end terminus – alveolus + alveolar duct, extends to resp bronchioles

Question 17

Diff between “pure chronic bronchtis” and “pure emphysema” (although both are typically seen in COPD)

Answer 17

• 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.

Question 18

What is centriacinar emphysema? Panacinar emphysema?

Answer 18

1. Diagram of normal structures within the Acinus (the fundamental unit of the lung).
   
   1. Terminal bronchiole (not shown) is immediately proximal to the respiratory bronchiole. & alv ducts & alveolus
2. Centriacinar emphysema: dilation that initially affects the proximal respiratory bronchioles.
3. Panacinar emphysema: initial distention of the peripheral structures (i.e., the alveolus and alveolar duct);
   
   1. 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

Question 19

How does tobacco lead to emphysema?

Answer 19

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
  • 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?

Question 20

Pathogenesis of COPD (emphysema and chronic bronchitis)

Answer 20

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

Question 21

Summary of all obstructive lung diseases?

Answer 21

1. Normal
   
   1. Goblet cell- mucous prod
2. Emphysema
   
   1. Some areas of normal alveoli and some alveoli without fibrosis but can see have disease
3. Chronic bronchitis
   
   1. Increase in inflammation of epithelium
   2. Increase in mucous formation and accumulation of mucous plugs
   3. Hyperinflated alveoli not collapse prop with exirpation
4. Bronchial asthma
   
   1. Degranulation of mast cell (IgE mediated resp to allergens in air)
   2. Some mucous
   3. Hyperinflation

Goblet cells=where muc formed

Question 22

What are pores of Kahn?

Answer 22

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

Question 23

Why do we encourage incenstive spirometer use?

Answer 23

• Pts w/ COPD – give IS postoperative– encourage deep breathing/pulm toilet so they can take deep breath & get air into alveoli that may be plugged by muc.
• If pts don’t do that→ get atelectasis & the alveoli collapse.
  
  • Over time, that can cause an increase in fluids bc the caps that feed those alv are dysfxntal and fluid extravasates from the caps into those areas of lungs.
    
    • This is why its important to provide adequate TV to pt
      
      • If tidal volumes (VT) small → can cause absorption atelectasis!

Question 24

What is bronchiectasis

Answer 24

• Localized, irreversible dilation of bronchus
• Due to inflammation-
  
  • Chronic bacterial infections that lead to inflammation of lungs
• Destruction of airways
  
  • Airways become thickened
• Pooling of mucus
• Bacterial superinfection
  
  • tough to eradicate → put on Long term antibiotics and with good AntiX (tough to get rid of)
• Diagnose:
  
  • chronic purulent cough, clubbing of fingers – clubbing of fingers over time bc the PaO2 is dec & not getting enough O2 to periphery
    
    • Irreversible dilation of bronchus (not bronchioles, larger portion more proximal to alveoli sit)

Question 25

What is cystic fibrosis?

Answer 25

several tx issues in epithelial cells (lungs, pancreas, liver, GI tract, reproductive organs) * Single gene on **Chromosome 7** * → Decrease in Na and H₂O transport in/out of cell-viscous secretions * Dehydrated **viscous secretions** that are associated with **luminal obstruction** * **luminal obstructions of various organs → pancreas, liver, GI, lungs** * Destruction and scarring of exocrine glands **w/ chronic pulmonary infections**- * Develop pneumonia, ventilator dependent → leading ultimately to mortality * Defective transport in epithelial cells of: * lungs – *not nec a lung dx per se but reason for such gr8 mortality in CF* * pancreas * liver * GI tract * Reproductive organs * **Diagnosis:** * **presence of Cl [] higher than 70mEq/L in sweat** – *skin test. Sweat glands don’t fxn properly either* not necessary lung disease, but lungs involved (mortality high bc of it)