Bronchodilators Flashcards
What are the uses of bronchodiltors?
Bronchodilators are used in Asthma and chronic obstructive airway disease
What is the most effect cure for COPD?
Oxygen
What is asthma?
Asthma is a chronic obstructive inflammatory airway disease of the airways commonly characterised by recurring symptoms, bronchospasms and reversible air flow obstruction
Which part of the nervous system is responsible for contraction/dilation of bronchioles?
Bronchoconstriction - Parasympathetic nervous system
Bronchodialtion - Sympathetic nervous system
Which neurotransmitter is released at the pre/post synaptic junctions of the PNS? And which receptors does it act on?
ACh is released. It acts on the M3 muscarinic receptors (post synaptic) and M2 muscarinic receptors (post synaptic).
How does ACh stimulate bronchoconstriction
ACh binds to the M3 muscarinic receptors on the Reissessen. This will contact a Gq protein - contact the PLC pathway and increase intracellular calcium to produce constriction of bronchioles. ACh also stimulates mucus secretion
How is excessive bronchoconstriction prevented?
ACh binds to the M2 post synaptic muscarinic receptors after binding to the M3 receptors. This inhibits the further release of ACh and hence prevents excessive bronchoconstriction. M2 receptors act as autoreceptors
Which neurotransmitter is released by sympathetic nervous system and produces bronchodilation? And which receptors does it bind to?
Adrenaline. It binds to the Beta 2 receptors
What is the effect of adrenaline?
Adrenaline is a Beta 2 agonist. It stimulates bronchodilation and inhibits histamine secretion from mast cells and mucus secretion. It is an anti-inflammatory
What are NANC dilators? Give 2 examples
Non adrenogenic, non cholinergic transmitters released by the Autonomic nervous system that produce vasodilation. examples: NO (nitrous oxide) and VIP
What is the role of sensory nerves?
Sensory nerves are important bronchi constrictors. They have C fibres and irritant receptors that cause local constriction during coughing, etc. They release substance P and neurokinin C for local constriction.
Give examples of inflammatory mediators for constriction of bronchioles
histamine, leukotrines, PAF
What are the 4 classes of bronchodilators?
- Beta 2 antagonists
- Muscarinic antagonists
- Xanthines
- PDE - 4 inhibitors
Name other anti - asthma/anti inflammatory drugs
Sodium Cromoglycate
anti inflammatory steroids
Anti - igE
omalizumab
Name 3 Beta 2 antagonists
- Salbutamol 2. Terbutaline 3. salmeterol (long lasting)
What are the effects of Beta 2 antagonists and how are they taken?
Beta 2 antagonists produce bronchodilation and may have an anti-inflammatory role. They are taken in orally for rapid action
What are the side effects of beta 2 antagonists and how are they produced?
- Tachycardia - There are some Beta 2 receptors near the AV node of the heart and the agonists may bind to this
- Headache - vasodilation
- Tremor - circulating adrenaline
- Anxiety - Caused by above 3 symptoms
What could happen as a result of taking the Beta 2 agonists orally?
They could cause irritation of the respiratory tract and may produce bronchoconstriction as a result
What could happen as a result of continuous usage of Beta 2 antagonists?
desensitizaiton
Which conditions are muscarinic antagonists used for?
Chronic obstructive airway disease or intractable asthma
Give examples of muscarinic antagonists
ipratropium ad oxitropium
How can muscarinic antagonists be taken?
They are inhaled
What is the advantage of muscarinic antagonists and what gives them this quality?
They have few side effects. This is because they are made of quaternary nitrogen which is very poorly absorbed into the system because it is permanently ionised.
Give 3 examples of xanthines
- Caffeine 2. Theophylline 3. Aminophylline
When and how are xanthines taken?
Xanthines are taken orally for prophylaxis - they are only given as prevention therapy - not for acute asthma
Are xanthines slow/fast acting?
They are slow acting and have a low therapeutic index
What is the range of dosage of xanthines? How much xanthines is considered toxic?
effective between 10 - 20 mg/litre
toxic >25 mg/litre
What are the side effects of xanthines?
Nausea, insomnia, convulsions, diuresis, headache and arrythmias
What are the two hypothetical mechanisms of xanthines?
- Inhibition of PDE. PDE stimulates breakdown of cAMP and cAMP increases levels of cGMP which is responsible for bronchoconstriction.
- Adenosine leaks out from compounds all the time and can cause bronchoconstriction. So xanthines inhibit adenosine receptors.
Give an example of PDE - 4 inhibitor
roflumilast.
What is the effect of PDE - 4 inhibitors?
They inhibit PDE. PDE stimulates breakdown of cAMP and cAMP increases levels of cGMP which is responsible for bronchoconstriction.
How are PDE - 4 inhibitors given?
They are given orally
What are the side effects of PDE - 4 inhibitors?
nausea, vormitting, insomnia, and headache
Why are PDE - 4 inhibitors not used?
This is because they tend to produce suicidal tendencies in patients
Give an example of a leukotrine antagonist?
Monteleukast
How do Leukotrines antagonists work?
Leukotrines are bronchoconstrictors and these antagonists bind to their receptors and inhibit them
When and how are leukotrine antagonists taken?
They are taken orally and are used in severe asthma or to prevent exercise induced asthma
What are the side effects of leukotrine antagonists?
Abdominal pain, headache,, respiratory tract infections and suicidal behaviours
