asthma COPD Flashcards
signs symptoms COPD
(productive) cough
dyspnoea gets worse over time
worse dyspnoea with exertion
FEV1/FVC in COPD
<0.7
pathophysiology COPD - which molecules, which impact(3)
- fibrosis smooth muscle
- emphysema (alveolar wall destruction)
- mucus hypersecretion
diagnostic differential asthma vs COPD
- Atopy/non atopy
- Allergy/not affected
- IgE/TH1 cytotoxic
- AHR/Not
- Eosinophil+Masts/ Neutrophils
- good days and bad days/ progressive
- good steriod response/poor
why do COPD pts end up in hosp
chest infections
2 assessment tools for COPD
GOLD, assesses FEV/FVC fraction
ABCD assesses severity of symptoms vs lung ftn
explain COPD ABCD assessment tool
Saba
Laba
Lama
Everything including ics
Group a and b 0-1 exacerbations not req hosp
Group c and d 2 mod or >1 hospital
consider ICS in COPD when
eosinophil count is high
mainstay trtment in COPD
LAMA or LABA
inflam genes affected by ICS
CXCL-8
TNF-alpha
IL-6
ICS in COPD increased risk of
pneumonia
steroid use risk factors
osteoporosis
skin
central adiposoty
what is bronchiectasis
chronic progressive
loss of wall
dilation of airways
mucus hypersecretion
irreversible
bronchiectasis = airway dilation so how come narrowed airway
hypersectretion of mucus, and can’t clear it - leads to increased LRTI
most common risk factor for bronchiectasis
frequent LRTI
most common comorbidities bronchiectasis
asthma
copd
also CF, IBS, RA
3+ exacerbations of COPD, suspect…
bronchiectasis
bronchiectasis signs and symptoms
8wks cough
much prurulent sputum
dyspnoea
diagnostic bronchiectasis
spirometry
Chest High Resolution CT
managemnet bronchiectasis
7-14d abx (correct one - sputum culture)
Pulmonary rehab - airway clearance
smoking cessatin
oral hydration
sometimes longterm abx
no ICS
is bronchiectasis reversible
no
2 key features of asthma
VARIABLE resp symptmos
VARIABLE exp airflow limitation
asthma triad symptoms
bronchospasm
mucus hypersecretion
airway inflam & remodelling
what common meds can trigger asthma
NSAIDS
where is asthma pathology
small airways
what is desquamation
IL-5 does what
triggers eosinophils -> mucus
What do IL4 and 13
drive IgE and mucus production
histamine causes…
smooth muscle to contract
3 most important interleukins in asthma
IL4, 5, 13
how can viruses affect asthma
Virus can activate the epithelium to release Alarmin cytokines e.g. TSLP to active T2 cells
what happens if TH2 immunity is upregulated
other sides of immunity are downregulated
tests to measure if TH2 immunity is activates
FeNO breeath test and raised eosinophilia
key in asthma diagnostic
variable episodic nature of symptoms
what is wheexe
polyphonic tones in wheeze
asthma diagnostic pathway
key feature on asthmatic flow volume curve
scalloping - then reversed somewhat by salbutamol
what improvement feature in asthma diagnosis
12% improvement with salbutamol
when is peak flow worst
4am
peak flow chart?
3 best attempts once on wakin and once mid afternoon
asthma management ladder
beta 2 agonists bind to
G coupled receptor
beta 2 agonists should be given with .. because..
steroids
effect is better and steroid blocks downregulation of b2 agonist receptors
how do MAbs work in asthma (2)
either bind eg IL33 or block receptor
high FeNO is marker of
IL4/IL13
what is MART inhaler
maintenance and relief.
steroid is combined with reliever