Pathophysiology of respiratory diseases pt 2 Flashcards
What is chronic obstructive pulmonary disease
-COPD= a mixture of chronic bronchitis and emphysema and encompasses a long term, progressive and accelerated decline in respiratory function
How does smoking reduce respiratory function and lead to COPD
-Nasty Chemicals Inhaled: Tobacco smoke is full of noxious chemicals and reactive oxygen species.
Defense System Weakened: Your lungs have a natural defense system to clean out debris like tiny hairs called cilia that move mucus. Smoking impairs this mucociliary clearance, making it harder to get rid of harmful stuff. Imagine the tiny cleaning crew in your lungs not working properly.
Tissue Damage: The constant irritation from the chemicals directly damages the lung tissue. It’s like constantly scratching a delicate surface – it gets worn down over time.
Inflammation Overdrive: Smoking triggers an inflammatory response in your lungs. Your body tries to fix the damage, but with ongoing smoking, this inflammation becomes chronic and harmful. It’s like a fire that keeps burning and causing more damage.
Enzyme Imbalance: Your lungs have enzymes that help keep things balanced. Smoking causes increased protease burden (more of the enzymes that break down tissue) and antiprotease inactivation (it weakens the enzymes that protect tissue). This leads to the destruction of the lung’s stretchy structures. Think of it like having more demolition crew and fewer builders in your lungs.
More Bad Guys Arrive: Smoking also activates and brings in more harmful immune cells like macrophages and neutrophils, which release even more damaging substances (like IL-8 and TNF-α) that worsen inflammation.
Long-Term Changes: Over a long time, this constant damage and inflammation lead to tissue remodeling. The structure of your lungs changes permanently, making them less stretchy and efficient. This is what happens in COPD.
More Infections: Because the cleaning system is broken and the lungs are damaged, smokers are also more prone to respiratory infections.
What pathological features are observed within the airways of COPD patients
-damage to cilia
-mucus hypersecretion (increased goblet cells)
-weakened airway structure and loss of patency
-impaired mucociliary clearance
-irritation of sensory neurones
-decreased luminal area
-emphysema (decreased surface area +perfusion)= decreased gas exchange
Loss of elastin fibres= increased compliance, decreased recoil
What are the effects of chronic respiratory failure on the body
-chronic alveolar hypoxia—-> hypoxic vasoconstriction —-> pulmonary hypertension —-> increased right ventricular afterload —-> right heart failure
-chronic alveolar hypoxia—> hypoxaeima, decreased exercise tolerance
What are two types of COPD
-emphysema
-chronic bronchitis
Explain what happens in emphysema
In emphysema:
The balloons get damaged and lose their stretchiness (↓ elastic recoil). This can even lead to them detaching from their blood supply (Alveolar detachment).
It’s harder to push air out, leading to air getting trapped in the lungs (Air trapping on expiration). People might use pursed-lip breathing to try and force the air out.
The lungs become more floppy and easier to inflate (↑ lung compliance), but this isn’t a good thing because they don’t recoil properly to push air out.
The network of tiny blood vessels around the air sacs gets destroyed (Destruction of capillary bed), reducing how much oxygen can get into the blood (↓ DLCO).
Initially, the oxygen levels in the blood might be okay until the later stages (Relatively well-oxygenated blood until late stage), but eventually, it becomes a problem.
Because it’s harder to breathe, the work of breathing increases, leading to symptoms like dyspnea (shortness of breath).
Over time, the chest can become barrel-shaped (Barrel chest).
Other problems like dyspnea, cachexia (muscle wasting), osteoporosis, and heart disease can develop.
Explain chronic bronchitis
In chronic bronchitis:
There’s airway obstruction, making it harder for air to flow in and out.
You might hear wheezing.
There’s mucus hypersecretion, meaning the airways produce a lot of thick mucus.
This leads to a productive cough with copious sputum (lots of phlegm).
The amount of air you can forcefully breathe out quickly (↓ FEV1) and the ratio of that to the total amount of air in your lungs (↓ FEV1/FVC) decrease.
The blocked airways can lead to low oxygen levels in the air sacs (Alveolar hypoxia).
What can both conditions lead to
Both conditions can lead to:
Ventilation-Perfusion (V/Q) mismatch: This means that some parts of the lungs are getting air but not enough blood flow, or vice versa, making oxygen transfer less efficient.
Low oxygen in the blood (Hypoxemia) and high carbon dioxide in the blood (Hypercarbia).
The body might try to compensate for low oxygen by making more red blood cells (Polycythemia), which can lead to a bluish discoloration of the skin (Cyanosis).
High carbon dioxide can lead to respiratory acidosis (the blood becomes too acidic).
Low oxygen can also cause the blood vessels in the lungs to narrow (Pulmonary vasoconstriction), leading to high blood pressure in the lungs (Pulmonary hypertension).
This increased pressure can strain the right side of the heart (↑ RV output - RHF), potentially leading to Cor pulmonale (right-sided heart failure) with symptoms like ↑ JVP (swollen neck veins), loud P2 (a heart sound), parasternal heave (a chest movement), and peripheral edema (swelling in the legs).
The body might also retain fluid (Fluid retention) through the activation of a hormone system (Activation of RAAS).
Both conditions also involve inflammation in the lungs.
Explain characteristics of pneumonia
pneumonia= infection of the lung parenchyma, resulting in inflammation and oedema
What is the Pathophysiology of pneumonia induced acute lung injury
Weakening of host defence (e.g.
following viral infection, damage to
epithelium, or immune suppression)
↓
Colonisation of alveoli by pathogens
↓
Activation of macrophages and
cytokine release (IL-6, IL-8, TNF-α)
↓
Recruitment of neutrophils into
alveolar space, release of proteases
& ROS
↓
Injury to alveolus and surrounding
structures (see next slide)
Explain how alveolar injury leads to impaired gas exchange and hypoxaemia
Alveolar injury:
Deposition of dead cells &
proteins in alveolar wall
(“hyaline membrane” formation)
Disruption of endothelium and
basement membrane disruption
Fluid accumulates in
alveoli and/or interstitium
Lung sounds
(crackles)
Impaired gas exchange
Lung opacity on X-ray
Hypoxaemia*
