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Respiratory System > 11. Lung Infection > Flashcards

11. Lung Infection Flashcards

1
Q

What percentage of people admitted to hospital with pneumonia die?

A

5%

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2
Q

What 3 types of defences are present in the respiratory tract?

A
  • Mechanical: URT filtration, mucociliary clearance, surfactant, epithelial barrier
  • Local - BALT, secretory IgA, lysozyme, transferring, antiproteinases, alveolar macrophages
  • Systemic - polymorphonuclear leucocytes, complement, immunoglobulins
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3
Q

How sterile is a healthy lung?

A

Sterile from the first bronchial division

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4
Q

Describe the overall structure of the ciliated epithilium

A
  • Tight junctions - cohesive layer
  • Ciliated cells and goblet cells
  • 200 cilia for 1 cell
  • Cilia surrounded by a watery periciliary fluid
  • Mucus floats on top of the cilia - sticky and gel-like
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5
Q

Describe the movement of the cilia

A
  • Beats 15 times per second - metachronal rhythm
  • Vertical, engages with mucus, pushes forward
  • Cilium withdrawn within the periciliary fluid in a curved fashion
  • Repeats
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6
Q

Describe the ultrastructure of a cilium

A
  • 9+2 microtubule structure
  • 9 outer microtubule pairs have dynein arms
  • Dynein arms have ATPase - energy for microtubules to move up and down
  • Central 2 microtubules are used as an axis to move against
  • People can be born with abnormalities
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7
Q

What are the 2 most common causes of acquired defects of the mucociliary system?

A
  • Cigarette smoking - destroy the cilia, makes mucus more viscous
  • Viral infection - destroy cilia, more watery mucus, separate tight junctions
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8
Q

Why can mucus become a yellow-green colour following a viral infection, despite feeling better?

A

A bacterial infection capitalises on the weakness of the respiratory epithelium

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9
Q

Describe the restoration of the cilia following an infection

A
  • Mucociliary system is disabled for around 6 weeks
  • Sometimes the cilia grow back abnormally (compound cilia are useless)
  • Most vulnerable in the first 3-4 days after infection
  • Fully defended after around 3 weeks
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10
Q

What generally causes acute, overwhelming respiratory infection syndromes?

A
  • Could be a very virulent bug

* Could be a host defence disorder

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11
Q

What generally causes recurrent-acute (slow to resolve) respiratory infection syndromes?

A
  • Bronchial
  • Pneumonic
  • Host defence abnormalities
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12
Q

How does phlegm react to antibiotics in respiratory infection syndromes?

A
  • Daily purulent sputum only temporarily responds to antibiotics
  • Daily yellow/green phlegm is unusual
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13
Q

What happens to the heart if the cilia don’t work?

A
  • Side of the body that the heart is on is random
  • 50% of people born without functioning cilia have dextrocardia (heart on right)
  • Microtubules used to guide cells during embryological development
  • Abnormality e.g. dynein arm defect - no outer dynein arm
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14
Q

How are defective cilia identified?

A
  • Biopsy from the nose - looked at under the microscope

* Painful and uncomfortable

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15
Q

How does the amount of nitric oxide differ in people with primary ciliary dyskinesia?

A
  • Primary ciliary dyskinesia - malfunctioning cilia
  • Less NO
  • Normal NO - no nasal biopsy needed
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16
Q

Give an example of a virulent and less virulent pathogenic species in a respiratory disease

A
  • Streptococcus pneumoniae - pneumonia

* Encapsulated haemophilius influenza - bronchitis/sinusitis

17
Q

How do bacteria avoid the movement of the cilia?

A
  • Hair like fimbriae
  • Act as anchors to the epithelial surface
  • Stick to damaged epithelium, not where there is cilia
18
Q

What are bacterial strategies to avoid clearance from the airways?

A
  • Exoproducts which impair mucuciliary clearance - slow and disorganise ciliary beat, stimulate mucus production, affect ion transport
  • Enzymes - break down local immunoglobulins
  • Exoproducts - impair leukocyte function
  • Adherence - increased by epithelial damage and tight junction separation
  • Avoid immune surveillance - using surface heterogeneity, biofilm formation, surrounding gel and endocytosis
19
Q

What can bacterial persistence lead to?

A
  • Lung abscess

* Chronic airway infection

20
Q

What causes bronchiectasis?

A
  • Chronic airway infection
  • Chronic inflammation
  • Progressive damage to wall
  • Brochiectasis - enlarged airway
21
Q

What does pneumonia look like on an X-ray?

A
  • White area

* Due to solid lung - alveoli full of pus (trying to fight infection)

22
Q

What are the clinical features of pneumonia?

A
  • Cough
  • Sputum
  • Fever
  • Dyspnoea
  • Pleural pain
  • Headache
23
Q

What causes the stabbing pleuritic chest pain?

A
  • Pain fibres on the surface of lungs

* Solid lung => inflammation reaches the periphery

24
Q

Describe streptococcus pneumoniae

A
  • Negatively charged polysaccharide capsule
  • Difficult to bind to the epithelium but more virulent
  • Can invade the bloodstream => systemic
  • Produces a toxin (pneumolysin) that punches holes in cells, killing them
25
Q

What causes gas trapping in the lungs?

A
  • Diseased lungs
  • Lost elasticity
  • Collapses back down
  • Closed airways traps air
  • Higher residual volume
26
Q

What does trapped air look like in medical imaging?

A

• String of pearls
- dilated airways strung together by scar tissue
• Whitening at the bottom of the dilations
- pooling of phlegm

27
Q

What are common complaints of patients with bronchiectasis?

A
  • Daily sputum production
  • Recurrent respiratory infections
  • Breathlessness
  • Fatigue
28
Q

How can you help someone remove excess phlegm and why is it important?

A
  • Postural physiotherapy at set points each day
  • Remove the stimulus for neutrophils to move in
  • Reduces inflammation
29
Q

What are the causes of chronic bronchial sepsis?

A
  • Congenital e.g. pulmonary sequestration (tissue not connected to pulmonary arterial blood supply)
  • Mechanical obstruction
  • Inflammatory pneumonitis e.g. gastric contents, caustic gas
  • Fibrosis
  • Postinfective
  • Impaired mucociliary clearance
  • Immune deficiency
30
Q

What can Marfan’s syndrome lead to in the lungs?

A

• Bronchiectasis
• Structures that make joints hyper-reflexive are also in the airways
(• Fibrillin 1 defect)

31
Q

Describe the cycle of infection and inflammation

A
  • Chronic infection
  • Chronic inflammation
  • Damage
  • Impaired lung defence
  • Further inflammation
  • Further damage
32
Q

What changes the protease anti protease balance?

A

• Most important mechanism in inflammation

  • Neutrophil phagocytoses the bacterium and produces proteases that kills it
  • Protease spills into surrounding secretions
  • Anti-proteases (alpha 1 antitrypsin) in the airways normally neutralise the protease to prevent damage
  • They can be overwhelmed by the proteases if there are too many neutrophils during chronic inflammation
  • Free proteases in yellow-green sputum
  • More epithelial damage => more frequent infections

Respiratory System (18 decks)

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