Respiratory Flashcards
Define Asthma
Chronic inflammatory disease of airways characterised by
1) Bronchial hyperresponsiveness to stimuli (t1)
2) Reversible and variable airflow obstruction
3) Inflammation of bronchi
Pathophysiology of asthma
- type 1 igE mediated hypersensitivity reaction to stimuli
- igE on mast cells activated -> cytokine ->
- Early phase: smooth muscle contraction, mucus production, bv permeability
- Late phase: Inflammation
- Long term: airway remodelling, BM thicken, collagen deposit = irreversible airflow restriction
Epidemiology of asthma
More common in boys as children and girls as adults
Likely larger genetic role as children and env as adults
Presentation of asthma and features of history
Wheeze
SOB
Chest tight
Cough
Diurnal variation (worse at night and early morning)
Triggered by or made worse by something
Variable, recurrent and frequent symptoms
History of allergies
Smoker or around them
Family history of atopy or asthma
Asthma :aetiology precipitating factors
genetic and environmental component (atopic triad)
hygiene hypothesis
2 types of triggers: inducer + provoke
INDUCER enhance inflammatory response (physical antigen). Intrinsic asthma, children more
- allergens, viral, occupation exposure
PROVOKER enhance bronchospasm. Extrinsic asthma
- excercise, cold air, emotions, drugs (NSAID/aspirin, beta blocker)
Clinical signs of asthma on examination
Expiratory wheeze (polyphonic)
Hyperinflated chest
May see pec/SCM hypertrophy in poor managed
NB Severe asthma = no wheeze, silent chest
Investigations for asthma
Peak flow- show variable airflow limitation
Spirometry - show obstructive, decreased FEV1 to predicted
CXR + FBC to rule out other pathology
Stepwise management of asthma and SE of BA, ICS
- Remove triggers, stop smoking, lose weight
- Step 1 - PRN ICS + SABA or PRN ICS(budesonide) + LABA(formoterol)
- Step 2 - latter of step 1 or daily ICS + PRN SABA
- Step 3 - daily ICS + daily LABA(salmeterol, formoterol) + PRN SABA or higher dose ICS+PRN SABA
- Step 4 - add oral corticosteroids like prednisolone
- Beclametasone = Clenil, Qvar
- Budesonide = Pulmicort
- SE: sore throat/oral thrush, osteoporsis high dose
Beta agonists - tachy, hypOK
- Target infalmm- Leukotriene receptor antagonist
- Oral monteleukast
- CI in pregnancy and liver disease
- Add on, can be combined w 3 if 4 fails
- SE: hypersensitivity, Gi SE
Define acute severe asthma
Any one of:
- Cannot complete sentences
- HR >= 110
- RR >=25
- PEF <50% of predicted
Life threatening:
- silent chest, exhaustion, confused
- Sp02 <92% Pa02< 8
- hypotensive
- PEF <33%
Management of asthma attack
- 15L non rebreathe (A-> E assess)
- Nebulised salbutamol or terbutiline
- IV prednisolone
- nebulised iprotroprium bromide (short antimuscarinic)
?. MgS04 aminophylline mechanical vent
aim: sats > 94%
Define COPD
Chronic, partly irreversible, progressive, airway obstruction due to airway and parenchyma damage
may be accompanied by hypersensitivity
encompasses:
- Chronic bronchitis
- Emphysema
Risk factors for COPD
- Smoking (majority)
- Occupational exposure- coal, silica, dust, textile
- Biomass/coal/fuels internationally
- Alpha-1 antitrypsin deficiency
Define chronic bronchitis + pathophysiology
Chronic bronchitis:
- chronic productive cough for 3 months each in 2 consecutive years with no other explanation for cough
Path:
inflammation, mucus hypersecretion + airway narrowing
Define emphysema
Abnormal permanent dilation of airways distal to terminal bronchioles + destruction of their walls without obvious fibrosis
How does smoking -> COPD (pathophysiology)
toxin -> macrophage/cd8 lymphocyte recruitment -> neutrophil response -> protease activation
protease -> mucus hypersecretion in chronic bronchitis or alveolar destruction in emphysema
alpha 1 antitrypsin usually inhibits neutrophil protease activity
Presentation of COPD px
- SOB, worse on exertion
- Chronic productive cough (quantify)
- Expiratory wheeze
- Weight loss
- May have astham overlap - diurnal variation
- Chronic hypoxoemic, shut down pul circ -> RHF signs raised JVP, peripheral oedema
- Peripheral cyanosis, barrel chest
Investigation for COPD
- spirometry FEV1/ FVC <0.7
- Severity = how reduced their FEV is
Also need to do:
Bedside sats
FBC (elevated hb and rbc)
CXR
ABG
ECG (RH strain)
CT - distribution of emphysema may indicated a1antitrypsin if > at bases
Management of COPD
conservative = smoking cessation, vaccines (flu, pneumococcal), pulmonary rehab,reduce occupation exposure
FIRST: SABA(salbutamol) or SAMA (iprotroprium)
then ? asthma
if no asthma then LABA (salmeterol, formoterol) + LAMA (tiotropium) + SABA - SAMA if on before
if asthma + ICS
can also try:
- oral PDE inhibitor, bronchodilator theophyline
- ? prophylactic abx and mucolytics
- ? LTOT
-? surgery
Management of COPD exacerbation
- oxygen (84-92)
- increase bronchodilator frequency
- Add oral prednisolone
- abx - amoxicillin, clarithromycin, doxycycline
- phsyio (sputum)
MAY need NIV for pxs in T2RF
Smoking cessation devices
lots of forms of NRT - lozynges, patches, vape
or prescribed drugs:
- Bupropion (zyban)- antidepressant which can help smoking cessation, CI: seizures
- Varenicline (champix) NRagonist, not for px with psychiatric problems
Define bronchiectasis
Abnormal and permanent dilation of airways leading to accumulation of secretions and secondary infection/inflammation
Causes of bronchiectasis
- Cystic fibrosis
- post infection
- idiopathic
Presentation of px with bronchiectasis
Chronic productive cough copious amounts
recurrent chest infections
may have haemoptysis, sob, wheeze
Investigating for bronchiectasis
HRCT is gold standard, will show dilation and wall thickening- signet ring
Sputum culture on exacerbation
CXR may be helpful
Management of bronchiectasis
- Physiotherapy
- smoking cessation
- vaccines
medical:
- abx
- bronchodilators/corticosteroids
- neb saline
- NIV
- may have surgical
Lung cancer risk factors
- SMOKING
- occupation exposure
- air pollution
- radiation
- idiopathic + post infectious pulmonary fibrosis
- rarely genetic
- can sporadically occur in young females
Types of lung cancer
4 types of primary bronchial carcinomas = 95% of all lung cancer. first 3 are NSCC
- Adenocarcinoma
- Squamous cell carcinoma
- Large cell carinoma (rarest)
- Small cell (oat) carcinoma
- Carcinoid tumour
Types of lung cancer other than bronchial
- Malignant mesothelioma of pleura
- Secondary to mets
Adenocarcinoma (most common NSCC)
- cancer of larger airway
- peripheral solid mass, may appear ground glass so appear as infection
- Arise from neuroendocrine cells so can -> paraneoplastic syndromes
- Most strongly assd with smoking
- Highly aggressive, poor prognosis, present with mets
- untreated median survival 6 weeks
Squamous cell carcinoma (NSCC)
- Central cavitating mass can be confused w abscess
- Used to be most common
-
most strongly assd with smoking
*
Presentation of px with lung cancer
- Persistent cough (>6w)
- Haemoptysis
- SOB
- Chest
- Unintentional weight loss
- Fatigue
- Lymphadenopathy
May present with signs of paraneoplastic syndrome
Cushing XS ACTH (esp oat)
SiADH (oat)
Hypercalcaemia (SCC)
Clubbing
Diagnosis for lung cancer
Tissue sampling (many methods depending on frailty and location) and then immunohistochemistry
Small cell carcinoma
Only 10% of lung cancers
strong smoking asscn
- massive mediastinal lymphadenopathy
- may cause SVCO
- Most present at stage 4, poor prognosis bc nearly always mets
Carcinoid tumour
- Very rare type of lung cancer
- no/little asscn with smoking
- well defined golf balls on x ray
- majority are localised therefore curable
Management of lung cancer
Local: radio, surgery + adjuvant chemo if adv on surg
Stage 4: palliative chemo, immuno, targeted molecular, maybe radio
Molecular targeted therapy target mutations in normal molecular processes that have enabled tumour growth
Immunotherapy targets tumours ability to evade T cell destruction
Mesothelioma
Tumour of pleura
NB rare cause, tumours of pleura are usually emtastatic adenocarcinoma
Presnets with SOB and chest pain!
asbestos exposure
poor prognosis
palliative chemo/radio