resp pharmacology Flashcards
What are three inhaled corticosteroids, their use, mechanism and side effects?
beclometasone, budesonide, fluticasone
regular preventer when reliever alone not sufficient
pass through plasma membrane and activate cytoplasmic receptor, the activated receptor then moves into the nucleus to modify transcription. they reduce mucosal inflammation, widen airways, reduce mucus therefore decrease symptoms and exacerbations
can cause local immunosuppressive action - candidiasis, hoarse voice, pneumonia risk possible
How do steroids work more generally including on genes and their pharmacodynamics?
they increase beta2 receptors and anti-inflammatory mediators, they decrease inflammatory mediators.
poor oral bioavailability as it undergoes almost complete first-pass metabolism
a lipophilic side chain is added which means slow dissolution in bronchial fluid
what are the 2 types of beta2 agonists, how do they work and what are the adverse effects?
SABA and LABA
major action on airway smooth muscle and increase mucus clearance by action of cilia. prevent bronchoconstriction prior to exercise
adrenergic - tachycardia, palpitations, anxiety, tremor
SVT, increased glycogenolysis, increased renin, muscle cramps with LABA
what are the 2 names of SABA and when are they taken?
salbutamol, terbutaline
only used p.r.n.
what are the 2 names of LABA, which is faster acting, what are they an add on therapy with, and can it be prescribed alone?
salmeterol, formeterol (faster)
add on therapy to ICS and p.r.n. SABA
no, only alongside ICS as increased risk of death alone as it can mask airway inflammation in attacks - you prescribe when not controlled on ICS
what is the name of an LTRA used, what is the mechanism and side effects?
montelukast
LTC4 is released by mast cells/eosiniphils = increased bronchoconstriction, mucus and oedema through CysLT1 which is a GPCR - LTRA block CysLT1
headache, GI upset, dry mouth, hyperactivity
what is the name of a long acting muscarinic antagonist used, what is the mechanism and side effects?
tiotropium
relatively selective for M3 and causes anticholinergic effects though inhibition of muscarinic receptors
dry mouth, urinary retention, dry eyes
what is the name of an adenosine receptor antagonist what is the mechanism and potential interactions?
theophylline
widens airways
it has a narrow therapeutic index so can cause potentially life threatening index
interactions with CYP450 inhibitors so increases concentration of theophylline
what is the name of oral steroids given for severe uncontrolled asthma?
prednisolone
what are some features of acute severe asthma?
unable to complete full sentences, peak flow 33-50%, RR >25, HR >110
what are some features of life threatening asthma?
peak flow <33%, O2 <92%, pO2 <8kPa, normal pCO2, silent chest, cyanosis, poor resp effort arrhythmia, exhaustion, altered consciousness, hypotension
what is the treatment for severe asthma including the next drugs used if poor response?
O2 to achieve 94-98%, high dose nebulised B2 agonist (O2 driven), oral steroid should be prescribed for 7-14 days along with ICS
SAMA - ipratroprium, nebulised alongside B2 agnostic if poor response alone (less selective for M3 receptors than LAMA)
then consider IV aminophylline (adenosine receptor agonist) if no success
in an acute exacerbation of COPD, what steps are taked?
nebulised salbutamol and/or ipratropium
if patient is hypercapnia/acidotic, nebuliser should be air-driven and not O2 driven
oral steroids can be less effective
antibiotics
review action plan
what are the main 3 options of inhaler?
pressurised metered dose inhalers - inhalation and actuation device
breath-actuated mPDI - automatic activation upon inhalation
dry powder inhalers - micro ionised drug plus carrier power, own inspiratory flow - fast deep inhalation
