Session 2- Asthma Flashcards
what is asthma?
Hyper-responsiveness of the airways to allergic or non allergic triggers, leads to recurrent episodes of reversible airways obstruction; characterised by bronchoconstriction, broncho mucosal inflammation and hyper secretion, which leads to SOB, wheeze, cough and chest tightness
What causes bronchoconstriction in allergic asthma?
2 IgE molecules crosslinked to mast cells causes them to degranulate and release histamines, prostaglandins, tryptase which all stimulate the smooth muscle to contract
what causes the mucosal inflammation in asthma?
mast cells (might be activated by IgE cross linking), Th2 and eosinophils release or cause the release of inflammatory mediators such as IL4,5,13 which increase vascular permeability which leads to oedema, warmth and redness and attracts other inflammatory cells
what things can the airways be hyper responsive to in asthma?
cold air
tobacco smoke
pollution
exercise
dust mites
mold
pet dander
pollen
how does asthma present?
cough, (normally non productive)
wheezing, (normally only on expiration)
SOB,
chest tightness
diurnal variation - peak flow worse in the morning
often personal history of atopic disorder (hay fever, eczema)
family history of atopy/asthma
often presents in childhood, but not always!/can get mixed with COPD in elderly
what is the differential diagnosis of a cough?
asthma
pneumonia
chronic bronchitis/COPD
bordetalla pertussis infection (whooping cough)
lung cancer extrinsic allergic alveolitis interstitial pulmonary fibrosis bronchiecstasis sarcoidosis TB
what is the differential diagnosis of SOB?
pulmonary embolism MI/ACS congestive heart failure anaemia pulmonary hypertension
asthma
pneumonia
COPD
pleural effusion
anxiety/panic attack
obesity
how do you diagnose asthma?
there is no gold standard, more of a clinical diagnosis
tests you can do involve: spirometry, peak flow reversibility testing, CXR, FeNO breath test (NO released in inflammation, but not specific) skin prick test to identify allergens, blood count for eosinophilia
in GP, if you expect asthmatic, give peak flow diary for 2 weeks, first week without salbutamol inhaler and second week with. should be diurnal variation and improvement with the inhaler.
how do you manage asthma?
Non pharmacological: avoidance of triggers to reduce flare ups
Pharmacological:
Adrenergic beta 2 receptor agonist - induces smooth muscle relaxation: Salbutamol inhaler
inhaled corticosteroid - reduce airways inflammation: Clenil inhaler (like beclamethosone)
LABA- long acting beta 2 agonist (salmeterol)
LAMA- long acting muscarinic agonist
anti- leukotriene drugs (montelukast)
daily steroid tablet
before moving someone up the list of drugs used to manage their asthma, what should you check?
ADHERENCE - when and how often they are taking them
TECHNIQUE- may need to use a spacer device
how does the beta 2 adrenergic receptor agonist work?
salbutamol
binds to the g protein coupled receptor
activates adenyl cyclase
produces cAMP
which activates protein kinase A
which decreases intracellular calcium and hyperpolarizes the smooth muscle cells
therefore they cannot contract and instead relax, so reduce the bronchoconstriction occurring in an acute asthma attack
side effects of salbutamol
hypokalemia - loss of K from the blood (hence why on the wards you treat someone with hyperkalemia with salbutamol)
tachycardia- as there are beta 1 receptors in the heart, therefore if at a high enough dose it loses selectivity for the beta 2 receptor and can activate the beta 1 receptors causing a positive inotropic and chronotropic effect.
in a consultation how would you assess the control of ones asthma quickly?
RCP 3 questions (royal college of physicians)
- are the asthma symptoms effecting your sleeping at night?
- are the asthma symptoms there during the day?
- are your asthma symptoms preventing you from carrying out your daily activities, i.e. housework/school?
what is samter’s triad?
aka NERD: NSAID exacerbated respiratory disorder
- asthma
- respiratory symptoms exacerbated by aspirin
- nasal polyps
name 3 drugs which may trigger/worsen asthma and how do they do it?
Beta blockers (high enough dose, lose selectivity for the beta 1 receptors in the heart, block the beta 2 receptors in the lungs which cause smooth muscle contraction- bronchoconstriction)
NSAIDs- inhibit COX enzyme so less prostaglandins are produced, but this means more pass down the lipo-oxygenase pathway to produce leukotrienes which also cause bronchoconstriction
ACE Inhibitors- common side effect is a cough. not really asthma related but can be confused with or still worsen symptoms. ACE enzyme not only converts angiotensin 1 to angiotensin 2, but also bradykinin into inactive peptides.
