Lung infection

Question 1

What is bronchectasis?

Answer 1

airways become scarred, widened and inflamed with thick mucous that the patient will struggle to clear; pockets of mucous form and harbour bacteria that can multiply without clearance leading to chronic infection - ability to clear mucous chronically damaged, so cannot clear infections (easily); physio to empty the phlegm can prevent bacteria pooling and limit infection/inflammation

Question 2

What causes bronchiecstasis?

Answer 2

• Infection (pneumonia, TB, whooping cough, etc)
• inflammation permanently destroys the elastic-like tissue and muscles surrounding the bronchi (airways), causing them to widen.
• abnormal bronchi then become filled with excess mucus, which can trigger persistent coughing and make the lungs more vulnerable to infection
• Cycle continues

Question 3

What is the pathogenesis of pneumonia?

Answer 3

streptococcus pneumoniae

Question 4

What are the symptoms of pneumonia?

Answer 4

coughing, sputum, fever and dyspnoea because the alveoli become filled with pus, meaning the lung becomes solid; peripheral inflammation leads to stabbing pleuritic chest pain - airways are not scarred and some effort can be made to clear infections

Question 5

What are the differences in pathogenesis of acute and chronic infection?

Answer 5

acute:
neutrophils secrete proteases to destroy microbes during inflammation and infection, and normally this is balanced by anti-proteases in the airways

chronic:
the number of neutrophils is so large that the anti-proteases are overwhelmed leading to increased free proteases causing damage to the airway epithelia (which in turn makes it easier to be infected, creating a vicious cycle)

Question 6

What are the host defenses against infection?

Answer 6

Mechanical defences: URtract filtration, mucociliary clearance, coughing

Local defences: antiproteases and alveolar macrophages

Systemic defences: polymorphonuclear granulocytes, complement and antibodies

BALT (Bronchus Associated Lymphoid Tissue): samples antigens inhaled through nose and produces antibodies against these

Muco-ciliary clearance: cilia in the airways beat metachronally to waft mucous containing microbes towards the throat (9 microtubule pairs with dynein arms that have ATPase, providing the energy to slide over each other, using the central pair as an axis to move against)

Question 7

What are acquired conditions of lung defense compromisation

Answer 7

viral infections can lead to destruction of the cilia and tight junctions between epithelial cells, before opportunistic bacteria invade; cilia must regrow, taking weeks, and can regrow as useless compound cilia

Question 8

What are congenital conditions of lung defense compromisation?

Answer 8

1. Microtubule abnormalities (congenital): abnormal microtubules can lead to non-functional cilia and dextrocardia because these guide cells during embryogenesis (so if dextrocardia identified, check cilia function)
2. Dynein arm defects (congenital): lack of outer dynein arm prevents the cilia from moving even if present - stopping mucociliary clearance
3. Primary ciliary dyskinesia (congenital): lack of nasal nitric oxide appears to cause malfunctioning cilia