respiratory Flashcards
describe escalating management options according to BTS guidelines for asthma in adults
- SABA
- SABA + low dose ICS
- SABA + low dose ICS + LABA
- SABA + high dose ICS + LABA (or 4th drug e.g LRTA, theophylline or LAMA)
- oral CS
what to do if oral CS do not work for asthma
if IgE mediated, add in e.g. Omalizumab
what kind of drug is salmeterol?
long acting beta2 agonist
5 areas in the chest/lung/pulmonary that can cause conditions and examples of them
airways - copd, asthma, bronchiecstasis
parenchyma - pulm fibrosis, emphysema, hypersen pneumonitis
pleura - pleural effusion, pleural malignancy, pleural thickening
vascular - PE, pulm hypertension
ventilation - sleep apnea, obesity hypoventilation, neuromuscular dz, thoracic cage abnormality
examples of obstructive and restrictive pulmonary conditiosn
obstructive - copd, asthma, bronchiecstasis
restrictive - pulm fib, neuromuscular abnormalities, thoracic cage abnormalities, obesity
what is the shape of a flow volume loop showing large airway obstruction and diffuse small airway obstruction
large obs - hamburger shape
small obs - large spike and quick drop
what can cause large airway obs and what can cause small airway obs
large - tracheal collapse
small - copd/asthma
what is transfer factor
how well alveoli are at transferring gas to caps
difference between TLCO and KCO
tlco tells whole lung
kco tells per unit of lung vol
difference between hrct and spiral/helical ct
hrct is high res, can see small detail
helical shows continuously, can spot small things
generally what conditions can be picked up on hrct and helical ct
hrct - pul fibrosis, bronchiecstasis
helical - PE
e.g. of occupational pneumoconiosis
silicosis from silica, coal, and asbestos
what is the lung function pattern of pneumoconiosis
restrictive
what is the effect of pneumoconiosis
small diffuse nodules that progresses to massive large fibrosis
how to diagnosis pneumoconiosis
imaging, biopsy
what is the difference between asbestos pleural plaques and pleural thickening
pleural plaques usually asymptomatic, does not progress
diffuse plueral thickening has effusion, symptoms of sob and restrictive lung function.
what is asbestosis
interstitial fibrosis due to asbestos inhalation
what are signs of asbestosis
fine inspiratory crackles
basal reticular shadowing on cxr
restrictive lung function
difference between occupational asthma and work aggravated asthma
aggravated asthma happens in pre-existing asthma, aggravated by exposure in work place
occupational asthma is new onset asthma, due to sensitisation of allergen encountered in work place
what are 3 pathological characteristics of asthma
chronic airway inflammation
hyperresponsiveness
reversible
difference between sensitiser induced occupational asthma and irritant induced occupational asthma
sensitiser - most common, symptoms occur 1-2 years after sensitisation, immunologically driven
irritant-induced – reaction to exposure to irritant gas, fumes, vapours,
common causative agents of occupational asthma
flour dust isocyanate (paints) cleaning products enzymes animals
difference between high molecular weight and low molecular weight allergens
high molecular weight allergens are usually proteins that trigger an IgE response.
low molecular weight agents are usually chemicals with no specific IgE antibody
examples of LMW allergen
isocyanates
acrylates (glue)
risk factors for occupational asthma
history of atopy.
smoking
history indications of occupational asthma
new work place - 1-2 years
symptoms better when away from work
other workers affected as well
what are the goals of investigation of occupational asthma
to find relationship between symptoms and occupation
what are some investigations that can be done to investigate occupational asthma
spirometry inhaler reversibility IgE tests, skin prick daily PEFR challenge tests FeNO tests sputum eosinophils
what does PD20 tell in challenge testing
the dose of stimulant needed to cause 20% drop in FEV1
management in occupational asthma
standard asthma guidelines
avoidance of allergen
Anti-IgE drug if appropriate
2 types of coal workers pneumoconiosis
simple and progressive massive fibrosis
describe simple pneumoconiosis
coal deposits in lungs, visible on CXR. symptoms depend on severity
what are 3 categories of simple pneumoconiosis
category 1 - few small nodular markings on CXR, lung field normal, no symptoms
category 2 - more small nodular opacities, some symptoms, can progress to PMF
category 3 - many small nodular opacities, lung markings partly or completely obscured. high risk of progression to PMF
what is progressive massive fibrosis
more severe coal workers pneumoconiosis
several round fibrotic masses, usually in upper lobes. some with necrotic cavities
what are 2 serum markers that are positive in coal workers pneumoconiosis
rheumatoid factor
anti-nuclear antibodies
what does CXR look like in coal workers pneumoconiosis
destruction of lung apices
emphysema
lung airway damage
what do respiratory investigations look like in coal workers pneumoconiosis
spirometry
flow volume loop
gas transfer
spirometry shows mixed restrictive and obstructive pattern
irreversible airflow limitation shown
reduced gas transfer
symptoms of progressive massive fibrosis in coal workers pneumoconiosis
moderate to severe dyspnea
cough (may be black)
respiratory failure
describe the pathophysiological characteristics of COPD
chronic airway inflammation
over production of mucus in airways
infiltration of lymphocytes
emphysema - alveoli destruction
describe the effects of cor pulmonale
right ventricle hypertrophy
ECG changes
peripheral edema
polycythaemia
why does cigarette smoking cause COPD
due to increased infiltration of neutrophil granulocytes caused by smoke. tips the balance towards protease production by neutrophils
why is alpha1 antitrypsin important in preventing COPD
it is an importan anti-protease that prevents destruction of airways
non-respiratory manifestation of COPD
cardiovascular effects hypertension osteoporosis metabolic disorders depression
signs of COPD
wheeze, tachypnea increased work of breathing hyperinflated chest poor chest expansion polycythaemia coarse flapping tremor
explain respiratory drive in COPD patients
in long standing COPD, patients body gets used to elevated CO2 levels, thus becoming dependant on hypoxaemia as a ventilary drive.
how is cor pulmonale treated
LTOT
how is COPD investigated and diagnosed
spirometry reversibility with inhalers CXR, CT haemoglobin levels ECG echo
what must be done in non-smokers when investigating copd
alpha1 antitrypsin levels
what can be seen on a CXR of a COPD patient
flattened diaphragm, bullae, overinflation of lungs
inhaler management of COPD
give SABA (salbutamol)
give LAMA or LABA
give ICS
other management in COPD
mucolytics
LTOT
annual flu vaccines
pulmonary rehab
how to treat excr of COPD
oxygen
antibiotics
oral steroids (short course)
neb bronchodilators
why does COPD cause hypoventilation?
because after prolonged periods of hypercapnia, body gets used to high CO2 levels. this causes a switch in ventilatory drive from the normal (high co2 levels), to the secondary drive which is hypoxaemia.
so in prolonged COPD, body stops hyperventilating because it is used to high CO2 levels. if too much oxygen is given, then central ventilatory drive is switched off, causing hypoventilation.
cause of obstructive sleep apnea
airway narrowing during REM sleep due to relaxed muscles
causes/risk factors of obstructive sleep apnea
pharyngeal narrowing - obesity, acromegaly, enlarged tonsils
nasal obstruction - nasal polyps, adenoids, rhinitis
respiratory depressant drugs - alcohol, sedatives, strong analgesics
symptoms of obstructive sleep apnea
sleepiness fatigue poor concentration snoring resuscitative grunts during sleep
process of diagnosis/investigations for obstructive sleep apnea
collateral history epworth sleepiness scale overnight pule oximetry inpatient studies blood gases
how many apneac episodes per hour would be diagnstic of obstructive sleep apnea?
10-15
management for obstructive sleep apnea
correct modifiable factors - weight, drugs
cpap, ent surgery
causes of hypoventilation
decreased central drive respiratory muscle weakness obstructive sleep apnea thoracic cage dysfunction obesity related
what can cause central alveolar hypoventilation
any neurological conditions, trauma, space occuyping lesions, CNS degenerative diseases, drugs
what is obesity hypoventilation syndrome
abnormal ventilatory drive, associated with BMI>30
what are features of obesity hypoventilation syndrome
awake hypercapnia
obesity
exclusion of other causes
consequences of obesity hypoventilation syndrome
blunted ventilatory drive
chronic hypercapnia
polycythaemia
right sided heart strain/failure (and complications)
e.g. of neuromuscular disorders causing hypoventilation
myaesthenia gravis, ALS, GBS, muscular dystrophy
people with neuromuscular disorders also have central drive dysfunction - T or F
F, usually intact
symptoms of hypercapnia
headaches - similar to raised ICP sleepiness altered GCS poor concentration Co2 retention flap
what is hypersensitivity pneumonitis
inflammatory response to inhaled antigens
what are some associations/causes of hypersensitivity pneumonitis
farmers lungs
bird fanciers
cheese worker
mushroom workers
what is the pathophysiology of hypersensitivity pneumonitis
inhalation of antigen into alveoli and small airways causes inflammatory recruitment of neutrophils, macrophages, lymphocytes. this causes granulomas and focal inflammation.
eventually leading to fibrosis and lung dysfunction
symptoms of hypersensitivity pneumonitis
systemic symptoms - fever, weight losss, fatigue, anorexia
dry cough, breathlessness,
signs of hypersensitivity pneumonitis
dry cough, wheeze, squeak, lung crackles
radiological findings in hypersensitivity pneumonitis
CXR - fluffy nodular shadowing with streaky shadows
HRCT - reticular, nodular and ground glass opacities
pulmonary function tests findings in hypersensitivity pneumonitis
restrictive with reduced TLCO
what other investigations can be done in hypersensitivity pneumonitis
FBC - raised PMNs
bronchoalveolar lavage - lymphocytes and granulocytes
antibody testing
differentials of hypersensitivity pneumonitis
occupational asthma
treatment of hypersensitivity pneumonitis
avoidance, steroids
what is sarcoidosis
multisystemic granulomatous disease of unkown cause, frequently affecting the lung
how is sarcoidosis often picked up
incidental on CXR
symptoms of sarcoidosis
often asymptomatic
can affect any system and cause any local symptoms
systemic - fatigue, weight loss, fever, night sweats, peripheral lymphadenopathy
respiratory - cough, breathlessness, chest pain
lung function tests signs in sarcoidosis
mixed restrictive and obstruction picture, often variable
what is a classical CXR finding of sarcoidosis
bilateral hilar lymphadenopathy
what would HRCT show in sarcoidosis
opacities around lung fissures, hilar and diffused micronodular opacities “starry sky”
how to diagnose sarcoidosis
biopsy through EBUS
differentials of blateral hilar lymphadenopathy
sarcoid
TB
lymphoma
carcinoma
idiopathic pulmonary fibrosis is an inflammatory process - T or F
F
how does IPF happen
unkown cause, but injury/insult cause fibrogenic secretions of alveoli causing fibrosis.
history pattern in IPF
often no PMH, no occupational exposure, progressive breathlessness.
what other conditions is IPF associated with
coeliac, UC, renal tubular acidosis
symptoms of IPF
dry cough, breathlessness, advanced cases lead to cor pulmonale
signs of IPF
finger clubbing, peripheral cyanosis, bi-basal fine crackles, reduced lung expansion, pattern
what is the classical CXR finding in IPF
ground glass appearance - reticular opacities
lung function testing picture in IPF
restrictive with reduced TLCO
what would ABG look like in IPF
type 1 respiratory failure
what can be found on HRCT of IPF
lower lobe reticular opacities
traction bronchiecstasis
treatment for IPF
none, supportive, oxygen, pulmonary rehab, transplant
