Drugs Flashcards
Where are beta2- receptors found?
in smooth muscle of the bronchi, GI tract, uterus and blood vessels.
How do beta2- agonists reduce breathlessness?
stimulation of beta2-receptor activates a signalling cascade (by increase in cAMP) that leads to smooth muscle relaxation –> improves airflow in contracted airways
What type of receptor is a beta2-receptor
a G protein-coupled receptor
name a short acting beta agonist
salbutamol, terbutaline
name a long acting beta agonist
salmeterol, formoterol
what makes a LABA long acting?
increased lipophilicity
Salmeterol is salbutamol with a long lipophilic chain attached to it
where are beta-1-adrenoceptors found?
the heart
where are beta-3 adrenoceptors found?
brown adipose tissue
Side effects of beta-agonists
Common fight/flight adverse effects: tachycardia, palpitations, anxiety + tremor.
also promote glycogenolysis
? tolerance
types of bronchodilators (3)
beta-agonists, muscarinic antagonists & methylxanthines
Another name for muscarinic antagonists
antimuscarinics
short acting muscarinic antagonist
ipratropium
long acting muscarininc antagonist
tiotropium
Mechanism of muscarinic antagonist for COPD
block ACh binding to muscarinic receptors (M3) –> blocks affects of ACh —> stopping excessive bronchocontriction
At what step in chronic asthma treatment do you potentially use a long acting antimuscarinic?
step 4, in addition to a LABA and high-dose inhaled corticosteroid
What do methylxanthines inhibit?
phosphodiesterase. Which is needed for the conversion of cAMP to 5’AMP.
So indirectly leads to elevations in cAMP –> increased smooth muscle relaxation
What is theophylline?
a non-selective PDE inhibitor
Has wide ranging SEs: GI, CVS, CNS
classes of steroid
sex (testes, ovaries)
corticosteroids (adrenal cortex)
types of corticosteroid
mineralocorticoids: aldosterone - Na+ retention
glucocorticoids: hydrocortisone - metabolic, anti-inflammatory
name some semi-synthetic glucocorticoids
prednisolone, budesoinde
corticosteroid mechanism of action
pass through plasma membrane + interact with receptors in the cytoplasm.
activated receptor then passes into nucleus to modify transcription of a number of genes
pro-inflammatory cytokines, interleukins and chemokines are down regulated whilst anti-inflammatory proteins are up.
this reduces mucosal inflammation, widens the airways and reduces mucus secretion, improving symptoms and receding exacerbations in asthma & COPD
AE’s of corticosteroids
immunosuppressive: oral candidiasis (thrush), hoarse voice, ?pneumonia in COPD
metabolic: osteoporosis + muscle wasting
What does GRE stand for?
glucocorticosteroid response element
they can increase transcription (+GRE) or decrease it (-GRE)
why are NSAIDs detrimental in asthma?
they inhibit COX, so there’s a build up of arachidonic acid, and then an increase in cos-leukotrines, which are very potent bronchoconstrictors!
stage 1 - 4 of asthma management
1: SABA
2: SABA + ICS
3: SABA + ICS + LABA
4: add prednisolone? long acting antimuscarinic?
How is COPD managed differently to asthma?
asthma = beta agonists + steroids COPD = beta agonists/muscarinic antagonists + steroids
