Respi - lung infection Flashcards

1
Q

defences of lung

A
  • ciliary action by resp epithelium pushing the microbes trapped by mucus
  • cough reflex
  • immune response: alveolar macrophages
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2
Q

infective lung diseases

A
  • bronchitis & bronchiolitis
  • pneumonia
  • tuberculosis
  • bronchiectasis
  • lung abscess
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3
Q

bronchitis & bronchiolitis

- 2 examples

A

bronchitis: infection of bronchi
bronchiolitis: bronchioles

virus:

  • RSV (resp syncitial virus)
  • influenza tracheobronchitis
  • measles/chicken pox: may also spread to lungs
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4
Q

pneumonia

+ types of pneumonia (7)

A

infective inflammation and consolidation of lung
airspaces get filled with inflammatory exudate -> becomes solid/airless

types of pneumonia

  • pneumonitis
  • bronchopneumonia
  • lobar pneumonia
  • community/hospital acquired pneumonia
  • aspiration pneumonia
  • atypical pneumonia
  • viral pneumonia
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5
Q

pneumonitis

A

inflammatory disease caused by interstitial inflammation - airways not inflammed yet

also caused by other allergens: toxins, drug reactions, irradiation (exposed to radiation)

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6
Q

bronchopneumonia
+ x-ray characteristics
+ who it affects commonly

A

pneumonic consolidation centered on bronchi -> spreads to involve adjacent alveoli
patchy suppurative inflammation
affects lower lobes more cause of gravity
- common in infancy and elderly

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7
Q

lobar pneumonia

- bacteria

A

rapid spread through alveolar spaces and bronchioles affecting the whole lobe
- strep pneumoniae/ klebsiella -> 1st line antibiotics treatment
prompt treatment!

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8
Q

community acquired pneumonia

- bacteria

A

gram POSITIVE bacteria

  • strep pneumonia (most common)
  • h.influenzae, legionella, mycoplasma, m.tuberculosis
  • viral pneumonia
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9
Q

hospital acquired pneumonia

A

gram NEGATIVE bacteria
- klebsiella, e.coli, pseudomonas
increased risk for pts who are ventilated and intubated
- intubation -> colonisation
BAL (bronchoalveolar lavage) sampling of sputum

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10
Q

increase risk of tuberculosis

A
  • diabetes
  • chronic lung disease
  • alcoholism
  • HIV infection
  • immunocompromised - opportunistic. even organisms w/ low pathogenicity
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11
Q

prevalence of TB

A

poverty
crowding
chronic debilitating disease

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12
Q

TB cause

A

mycobacterium TB (rod)

  • inhaled
  • waxy cell wall: resistant to destruction by neutrophils
  • susceptible to macrophages, but can still proliferate
  • ZN stain positive
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13
Q

primary TB

+ possible outcomes (3)

A

no previous exposure
inhaled -> lymph nodes at lung hilum** (enlarges w/ granulomatous inflammation n caseation + undergo necrosis)

commonly exists as latent TB & stays dormant
may progress to miliary TB if it erodes through blood vessel
Resolution

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14
Q

secondary TB

+ outcomes of healing

A

previous exposure and sensitised
affects immunocompetent adults
- lesion at apex of lung** (further inwards)
may cause tissue destruction -> cavitation

healing:
- leaves area of caseous necrotic material surrounded by thick collagenous wall w/ calcification
- may remain latent but spread when pt becomes immunocompromised
- > destruction of lung tissue, erosion into blood vessels & airways
- > bronchopneumonia/ miliary TB

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15
Q

complications of TB

A
  • spread into pleural space via bronchi/ lymphatics

- enters the blood: miliary TB -> spread to pulmonary circulation - can even affect multiple organs

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16
Q

immunity against TB

A

Granulomatous inflammation -> Formation of granulomas
CD4+ T cells secrete cytokines and activate macrophages to kill the bacteria -> formation of epithelioid macrophages and multinucleated giant cells
- ADR: hypersensitivity, tissue destruction

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17
Q

miliary TB

A

appearance on X-ray: white tiny spots distributing the entire lung

18
Q

aspiration pneumonia

  • cause
  • progression
A

affects unconscious pts/ impaired swallowing
infection by anaerobes/ oropharyngeal bacteria
inhalation of gastric contents

may lead to formation of lung abscesses

19
Q

atypical pneumonia

  • bacteria
  • clinical and X-ray presentation
A

infiltration of the alveolar interstitium by chronic inflammatory cells
- mycoplasma, chlamydia, rickettsia

presents w/ pneumonia symptoms
X-ray: absence of consolidation

20
Q

viral pneumonia

A

influenza: H5N1, SARS, COVID-19

21
Q

HIV infection causing lung disease

- progression

A

opportunistic infection: PCP (pneumocystis carinii)
difficult to diagnose and control

may develop into cancer (lung cancer, Kaposi sarcoma, non-hodgkin lymphoma)

22
Q

bronchiectasis

+ characteristics

A

permanent abnormal dilation of main bronchi

  • purulent secretions
  • chronic inflammation of wall
  • loss of normal resp epithelium

may have recurrent infection
may present w/ haemoptysis
infection may spread to surrounding lung

23
Q

bronchiectasis pathogenesis

2 main factors

A

problem w/ drainage of secretions

  • obstruction of airway
  • viscous mucus (cystic fibrosis)
  • immotile cilia

recurrent and persistent infection

24
Q

bronchiectasis complications

A
  • chronic suppurative inflammation
  • lung abscess
  • hematogenous spread of infection
  • secondary amyloidosis
  • cor pulmonale -> RHF
25
Q

lung abscess

- causes (5)

A

localised area of suppurative necrosis -> form large cavities

infection causes:

  • pulmonary infarction
  • aspiration of infective material - infection through the airways
  • bronchial obstruction -> occlusion of airways
  • bronchiectasis
  • staph aureus
26
Q

complications of lung abscess (4)

A
  • septic embolism : formed by multiple abscesses
  • rupture into pleura : empyema (pus), pneumothorax (air)
  • erosion into pulmonary vessel -> haemorrhage
  • bacteremia (bacteria entering the bloodstream)
27
Q

respiratory illnesses in children

A

developmental:

  • bronchial atresia
  • bronchogenic cysts
  • bronchopulmonary sequestration

neonatal respiratory distress syndrome (NRDS)

affecting lungs:

  • immotile cilia syndrome
  • cystic fibrosis
28
Q

bronchial atresia

A

tube like structure of airways not formed properly

29
Q

bronchogenic cysts

A

parts of the bronchial that is sealed off from the rest of the airway

30
Q

bronchopulmonary sequestration

A

portion of lung that does not communicate w/ normal bronchial tree

31
Q

neonatal respiratory distress syndrome (DRTS)

  • pathogenesis
  • effects
A

deficiency of surfactant (produced by type 2 pneumocytes) in the lungs
- high surface tension in the alveoli -> cannot be kept open -> alveolar collapse
hyaline membranes present

effects:
- hypoxia
- damage to endothelial and alveolar lining cells

affects premature babies

32
Q

immotile cilia syndrome

A

cilia has abnormal structure/
cilia does not move in coordination
the foreign body just gets stuck there and wont get swallowed/ removed -> risk of recurrent infections

33
Q

cystic fibrosis

- more common in what race

A

production of viscous mucus that cannot be cleared from lungs/pancreas/intestines

  • > mucus remains stagnant
  • > repeated infections / bronchiectasis
  • > resp failure

affects Caucasians more - autosomal recessive disorder

34
Q

4 stages of inflammatory response in lobar pneumonia

A
  1. Congestion
  2. Red hepatisation (presence of RBC, neutrophils)
  3. Grey hepatisation (RBC broken down already, left fibrino exudate)
  4. Resolution
35
Q

Complications of pneumonia

A
  • spread locally: lung abscess
  • spread dismally: septicemia
  • empyema - rupture of purple not fluid into pleural cavity
36
Q

Clinical manifestations of bronchopneumonia

A
  • mucopurulent sputum and cough

- acute high fever

37
Q

Clinical manifestations of pulmonary TB

A

Haemoptysis (coughing blood)
Chest pain
X-ray: nodular lesions - hilum / lung

38
Q

TB histological features (4)**

A
  1. CD4+ T lymphocytes
  2. Epithelium histeocytes (granuloma)
  3. Multinucleated giant cell
  4. Central caseating necrosis
39
Q

Clinical features of bronchiectasis

A
  • crackles in breathing w/ high and low pitch breath sounds (esp during expiration)
  • mucopurulent foul smelling sputum
  • breathlessness
  • hemoptysis (coughing blood)/ blood in sputum
40
Q

treatment of TB

A
  1. Damage already done
    - contact prophylaxis with isoniazid
    - isolate and monitor
  2. Preventing future damage
    - 2 months of isoniazid, rifampicin, pyrazinamide, ethambutol (RIPE)
    - follow up with 4 months of isoniazid, rifampicin
    - Isolate and monitor
    - observe sputum conversion, weight gain
    - can go back to community with directly observed therapy until treatment regimen is complete