Respi - lung infection Flashcards
defences of lung
- ciliary action by resp epithelium pushing the microbes trapped by mucus
- cough reflex
- immune response: alveolar macrophages
infective lung diseases
- bronchitis & bronchiolitis
- pneumonia
- tuberculosis
- bronchiectasis
- lung abscess
bronchitis & bronchiolitis
- 2 examples
bronchitis: infection of bronchi
bronchiolitis: bronchioles
virus:
- RSV (resp syncitial virus)
- influenza tracheobronchitis
- measles/chicken pox: may also spread to lungs
pneumonia
+ types of pneumonia (7)
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
pneumonitis
inflammatory disease caused by interstitial inflammation - airways not inflammed yet
also caused by other allergens: toxins, drug reactions, irradiation (exposed to radiation)
bronchopneumonia
+ x-ray characteristics
+ who it affects commonly
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
lobar pneumonia
- bacteria
rapid spread through alveolar spaces and bronchioles affecting the whole lobe
- strep pneumoniae/ klebsiella -> 1st line antibiotics treatment
prompt treatment!
community acquired pneumonia
- bacteria
gram POSITIVE bacteria
- strep pneumonia (most common)
- h.influenzae, legionella, mycoplasma, m.tuberculosis
- viral pneumonia
hospital acquired pneumonia
gram NEGATIVE bacteria
- klebsiella, e.coli, pseudomonas
increased risk for pts who are ventilated and intubated
- intubation -> colonisation
BAL (bronchoalveolar lavage) sampling of sputum
increase risk of tuberculosis
- diabetes
- chronic lung disease
- alcoholism
- HIV infection
- immunocompromised - opportunistic. even organisms w/ low pathogenicity
prevalence of TB
poverty
crowding
chronic debilitating disease
TB cause
mycobacterium TB (rod)
- inhaled
- waxy cell wall: resistant to destruction by neutrophils
- susceptible to macrophages, but can still proliferate
- ZN stain positive
primary TB
+ possible outcomes (3)
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
secondary TB
+ outcomes of healing
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
complications of TB
- spread into pleural space via bronchi/ lymphatics
- enters the blood: miliary TB -> spread to pulmonary circulation - can even affect multiple organs
immunity against TB
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
miliary TB
appearance on X-ray: white tiny spots distributing the entire lung
aspiration pneumonia
- cause
- progression
affects unconscious pts/ impaired swallowing
infection by anaerobes/ oropharyngeal bacteria
inhalation of gastric contents
may lead to formation of lung abscesses
atypical pneumonia
- bacteria
- clinical and X-ray presentation
infiltration of the alveolar interstitium by chronic inflammatory cells
- mycoplasma, chlamydia, rickettsia
presents w/ pneumonia symptoms
X-ray: absence of consolidation
viral pneumonia
influenza: H5N1, SARS, COVID-19
HIV infection causing lung disease
- progression
opportunistic infection: PCP (pneumocystis carinii)
difficult to diagnose and control
may develop into cancer (lung cancer, Kaposi sarcoma, non-hodgkin lymphoma)
bronchiectasis
+ characteristics
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
bronchiectasis pathogenesis
2 main factors
problem w/ drainage of secretions
- obstruction of airway
- viscous mucus (cystic fibrosis)
- immotile cilia
recurrent and persistent infection
bronchiectasis complications
- chronic suppurative inflammation
- lung abscess
- hematogenous spread of infection
- secondary amyloidosis
- cor pulmonale -> RHF
lung abscess
- causes (5)
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
complications of lung abscess (4)
- septic embolism : formed by multiple abscesses
- rupture into pleura : empyema (pus), pneumothorax (air)
- erosion into pulmonary vessel -> haemorrhage
- bacteremia (bacteria entering the bloodstream)
respiratory illnesses in children
developmental:
- bronchial atresia
- bronchogenic cysts
- bronchopulmonary sequestration
neonatal respiratory distress syndrome (NRDS)
affecting lungs:
- immotile cilia syndrome
- cystic fibrosis
bronchial atresia
tube like structure of airways not formed properly
bronchogenic cysts
parts of the bronchial that is sealed off from the rest of the airway
bronchopulmonary sequestration
portion of lung that does not communicate w/ normal bronchial tree
neonatal respiratory distress syndrome (DRTS)
- pathogenesis
- effects
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
immotile cilia syndrome
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
cystic fibrosis
- more common in what race
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
4 stages of inflammatory response in lobar pneumonia
- Congestion
- Red hepatisation (presence of RBC, neutrophils)
- Grey hepatisation (RBC broken down already, left fibrino exudate)
- Resolution
Complications of pneumonia
- spread locally: lung abscess
- spread dismally: septicemia
- empyema - rupture of purple not fluid into pleural cavity
Clinical manifestations of bronchopneumonia
- mucopurulent sputum and cough
- acute high fever
Clinical manifestations of pulmonary TB
Haemoptysis (coughing blood)
Chest pain
X-ray: nodular lesions - hilum / lung
TB histological features (4)**
- CD4+ T lymphocytes
- Epithelium histeocytes (granuloma)
- Multinucleated giant cell
- Central caseating necrosis
Clinical features of bronchiectasis
- crackles in breathing w/ high and low pitch breath sounds (esp during expiration)
- mucopurulent foul smelling sputum
- breathlessness
- hemoptysis (coughing blood)/ blood in sputum
treatment of TB
- Damage already done
- contact prophylaxis with isoniazid
- isolate and monitor - 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
