Respiratory Flashcards
severity of ARDS
depends on hypoxaemia
mild: PaO2 > 200
mod: PaO2 100-200
severe: PaO2 < 100
actions of alpha 1 antitrypsin
defends against neutrophil elastase
types of asbestos lung disease
pleural plaques
pleural thickening (mostly at bases, restriction and reduced compliance, reduced total lung capcity, normal KCO)
pleural effusions (often spontaneously resolve, usually exudate)
asbestosis
lung ca
treatment of mesothelioma
talc or indwelling pleural catheters for symptomatic effusion
RTx, CTx (non curative)
surgery potentially curative
hard metal lung disease
caused by cobalt dust
from making cutting tools or jet engine parts
> fibrosis
multi nucleated giant cells in alveoli with granulomas
Aspergillus species
over 200
Aspergillus fumigatus causes 70% aspergillosis
A terreus resistant to amphoteracin B and has poor prognosis
Aspergillosis disease patterns
- invasive
- ABPA
- chronic pulmonary aspergillosis (CPA)
- isolated infection
invasive aspergillosis
spores germinate into hyphae in immunocompromised
> invade parenchyma
> inflammation, thrombosis, infarction)
> haematogenous dissemination to brain, skin, eyes, heart, kidney, liver, spleen, GI , bone
ABPA
hypersensitivity to antigens from Aspergillus
typically CF and asthma pts
type I and type III
bronchiectasis and airway obstruction
chronic pulmonary aspergillosis
destructive infection
> fibrosis and loss of lung tissue
aspergilloma (assoc w/ TB)
aspergillus nodule
chronic cavitary (usually immunocompetent)
chronic necrotising (assoc with COPD and ETOHXS)
aspergillus isolated infection
nails, eyes, skin, sinuses, ear canals
endocarditis
endophthalmitis
diagnosing invasive aspergillosis
positive serum aspergillus galactomannan
serum 1-3 beta D glucan (not specific for aspergillus)
PCR RNA
HRCT chest
HRCT or MRI sinuses, brain
ABPA diagnosis
total IgE antibodies
aspergillus specific IgE and IgG
positive weal and flare skin test
eosinophilia
CXR infiltrates, bronchiectasis
HRCT mucoid plugging, infiltrates and bronchiectasis
chronic pulmonary aspergillosis diagnosis
IgG
CXR and HRCT- upper lobe mobile mass with air crescent, multiple nodules and cavities
treating invasive aspergillosis
amphoteracin B or echinocandin (caspofungin)
colony stimulating factors
isavuconazole, voriconazole 3/12
prophylaxis posaconazole
surgery if lesions continuous with great vessels of pericardium or severe haemoptysis from single cavity
asthma lung function tests
increased volume, reduced FEV1 and FEV1: FVC ratio < 70%
variable PEFR > 20%
improved PEFR > 15% after bronchodilator or steroids
berylliosis
looks similar to sarcoid
non caseating granulomas in lungs and nodes
surrounding fibrous tissue
CXR: fine nodulation evenly distributed throughout and b/l hilar lymphadenopathy
> progressive SOB and RHF
causes of bronchiectasis
LRTI
idiopathic
Marfans, Williams Campbell
HIV, haem malignancy, post transplant
RA, sjogren
IBD
ABPA, CF
obstructed or compressed bronchus (malignancy)
chemical pneumonitis
primary ciliary dyskinesis, kartagener, young
A1AT
asthma management
SABA for everyone
add ICS
> add LRTA or LAMA
COPD management
- SABA or SAMA
2a. (no asthma/steroid responsiveness) LABA + LAMA
2b. LABA + ICS - LABA + LAMA + ICS
remove ICS if it is not helping
indications for transplant in COPD
< 65y and:
- FEV1 and DLCO < 20% predicted
- history of hospitalisation w/ acute hypercapnia
- pulmonary HTN and/or cor pulmonale despite oxygen therapy
assessing COPD prognosis
BODE for 2y mortality
BMI, airflow Obstruction, Dyspnoea, Exercise
Decaf for inpatient mortality
Dyspnoea, Eosinophils < 0.05, Consolidation, Acidaemia, AF
simple vs progressive coal workers pneumoconiosis
simple:
small, asymptomatic round opacities
upper zones
focal emphysema
progressive:
nodule aggregation into larger opacities
possible cavitating lesions
Caplan syndrome
multiple round nodules in patients with seropositive RA with coal workers pneumoconiosis
in peripheral crops