Airway disease Flashcards
what are three forms of obstructive airway syndrome
asthma, chronic bronchitis, emphysema
what determines whether it is restrictive of obstructive
airways= obstructive lungs= restrictive
what is ACOS
asthma/ COPD overlap syndrome; COPD with reversibility and eosinophilia that respond to steroids
who gets ACOS
long standing smokers
what inflammatory agent causes asthma
eosinophils
what causes chronic bronchitis and which inflammatory agent in involved
smoking
neutrophils
what is emphysema due to and how is it characterised
due to destruction of alveolar walls leading to loss of alveolar support and collapsing
which division of the airways starts the conducting/as exchange section of the lungs
after 17
what maintains the integrity of the alveoli
alveolar walls
what does onset mean
age in which it started
what is atopic asthma
caused by an allergen
what is intrinsic asthma
no obvious extrinsic trigger involved
what is extrinsic asthma
caused by extrinsic trigger factor
what is airway hyperresponsiveness
when the airways are excessively twitchy to stimuli
what does chronic airway inflammation lead to
exacerbations and airway hyper responsiveness
what airway remodelling lead to
fixed airway obstruction
describe remodeling and how it is prevented
collagen deposition, thickening, hypertrophy;
via treatment
what can monocolonal antibodies target
leukotrine D4, LT3,4,5, histamine, IgE
describe two pathological features of severe asthma
epithelial shedding, mucus plugging
what follows (3) the inhalation of noxious substances that results in COPD
inflammation, mucociliary dysfunction, tissue damage
what are the characteristics of COPD
reduced lung function and exacerbations
what are the symptoms of COPD
breathlessness and reduction in quality of life
when can inflammation of the lungs lead to COPD
when normal repair/ protective mechanisms are overwhelmed or defective
describe the 5 pathological features of chronic bronchitis
chronic neutrophilic inflammation, mucus hypersecretion, mucociliary dysfunction, altered lung microbiome, smooth muscle spasm and hypertrophy, partially reversible
describe the 4 pathological characteristics of emphysema
alveolar destruction, impaired gas exchange, loss of bronchial support, irreversible
what are the symptoms of COPD
chronic- not episodic, non-atopic, daily productive cough, progressive breathlessness, frequent ineffective exacerbations
what is a specific symptom of chronic bronchitis
wheezing
what is a specific symptom of emphysema
reduced breath sounds
what is the chronic cascade in COPD
progressive fixed airflow obstruction, impaired alveolar gas exchange, respiratory failure, right ventricular hypertrophy/failure, death
describe how ACOS is diagnosed
COPD with blood >3% eosinophilia, more reversible to salbutamol
what are the 4 non pharmacological managements for COPD
stopping smoking, immunisation, physical activity, oxygen
what are the 4 pharmacological treatments for COPD
LAMA or LABA mono,
LABA/LAMA combo,
ICS/LABA combo,
ICS/LABA/LAMA combo
Asthma vs COPD
caused by smoking
COPD
Asthma vs COPD
allergic
asthma
Asthma vs COPD
only late onset
COPD
Asthma vs COPD
intermittent not chronic
asthma
Asthma vs COPD
non productive cough
asthma
Asthma vs COPD
non progressive
asthma
Asthma vs COPD
neutrophillic inflammation
COPD
Asthma vs COPD
eosinophillic inflammation
asthma
Asthma vs COPD
diurnal variability
asthma
Asthma vs COPD
poor corticoidsteriod response
COPD
Asthma vs COPD
good response to bronchodilators
asthma
Asthma vs COPD
reduced FVC and TLCO
COPD
Asthma vs COPD
impaired gas exchange
COPD
what does DLPD stand for
diffuse parenchymal lung disease
what are 3 causes of thoracic restriction outwith the lungs
skeletal; curved spine, deformity, broken ribs
muscle weakness; intercostal or diaphragmatic
abdominal obesity/ascites; compression of thoracic contents
describe the causes of thoracic restriction due to disease within the lungs
disease of alveolar structures; alveolar walls/lumen, ipaired gas exchange
what are the three classifications of chronic DLPD
due to occupational pr environmental agents or drugs, with evidence and without evidence of systemic disease
describe the gas exchange of O2 and CO2 in restrictive thoracic disease
impaired alveolar barrier to O2 gas exchange decreased PaO2
CO2 unchanged as alveolar ventilation the same and solubility of CO2 v high
describe the cause of DLPD
fluid in the alveolar air sacs; cardiac pulmonary oedema- due to increased PO venous pressure or
non cardiac po oedema- normal pressure with leaky vessels due to sepsis or trauma
what does ARDS stand for
acute respiratory distress syndrome
what is the consolidation of alveolar air spaces
when regions of lung tissue fill with fluid
what diseases can cause consolidation
infective pneumonia, infarction (interruption of blood supply e.g pulmonary emboli), BOOP (bronchitis obliterans organising pneumonia), COP (cryptogenic organising pneumonia)
what is an alveolitis
inflammatory infiltrate of alveolar walls
in terms of an alveolitis what is farmers lung
extrinsic-allergic-alveolitis
farmers lung is an example of a granulomatous-alveolitis, name another
sarcoidosis
what is a type 1/3 allergic response composed of mediated by
eosinophils
mediated by IgE
what else can cause alveolitis (4)
drug, fumes, pulmonary fibrosis, autoimmune
what is a glandular adenoma
a cancer that metastasises via lungs or lymph nodes to the lungs
what are the two categories of dust disease
fibrotic (lays down collagen) and non fibrotic
what is it called when a cancer causes DPLD
carcinomatosis
give the four things that cause an eosinophilic type 1/3 allergic response
parasites, drug, fungal, autoimmune
what is the clinical presentation of DLPD
breathless on exertion, cough no wheeze as no obstruction to airflow, finger clubbing, inspiratory lung crackles, central cyanosis (if hypoxaemic), pulmonary fibrosis- end stage f chronic inflammation
what are the other causes of finger clubbing (4)
inflammatory heart/bowel disease, liver disease, lung cancer, interstitial lung disease
what are crackles the sound of
the alveolar opening
what does DLCO stand for
diffusion lung capacity of oxygen
true or false; inhaled steroids are effective in the treatment of interstitial lung disease
false- not effective
what type of steroids should be used to treat interstitial lung disease
oral/systematic
what type of drugs dissolve collagen
don’t exist
what can slow the process of fibrosis
drugs
what are two antifibrotic agents
pirfenidone, nintedanib
is fibrosis completely irreversible
yeah
how can history be used to diagnose DLPD
occupation, pets, drugs, arthritis
how can lung volumes show a patient has DLPD
reduced lung volumes;
reduced FEV1
reduced FVC
normal ratio >75%
diangosis- what is peak flow like in DLPD
normal
diagnosis- how if DLCO in DLPD
reduced
diagnosis-what is arterial saturation like in DLPD
decreased PaO2 and SaO2
can an x-ray be used to diagnose DLPD
yes
how can an echocardiogram diagnose DLPD
exclude heart failure and diagnose secondary pulmonary hypertension
what immunolgical component can be used to diagnose DLPD
antibodies
how can an a CT scan be used in the diagnosis of DLPD
distinguishes between inflammatory ground glass and fibrotic nodular component in alveolar infiltrates
is ground glass opacity treatable
yes
how is DLPD treated
removal of allergen, treat any reversible alveolitis (e.g. ground glass in HRCT) via immuno-suppressants,
1st line treatments= systemic steroids,
2nd line treatment= steriod sparing (e.g oral Azathioprine),
what is IPF
idiopathic pulmonary fibrosis
how is IPF treated (holistic)
anti-fibrotic agents, O2 if hypoxaemic, treatment of secondary po hypertension, last resort lung transplant
what does idiopathic mean
unknown cause