Bronchodilators Flashcards

1
Q

What are the uses of bronchodiltors?

A

Bronchodilators are used in Asthma and chronic obstructive airway disease

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2
Q

What is the most effect cure for COPD?

A

Oxygen

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3
Q

What is asthma?

A

Asthma is a chronic obstructive inflammatory airway disease of the airways commonly characterised by recurring symptoms, bronchospasms and reversible air flow obstruction

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4
Q

Which part of the nervous system is responsible for contraction/dilation of bronchioles?

A

Bronchoconstriction - Parasympathetic nervous system

Bronchodialtion - Sympathetic nervous system

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5
Q

Which neurotransmitter is released at the pre/post synaptic junctions of the PNS? And which receptors does it act on?

A

ACh is released. It acts on the M3 muscarinic receptors (post synaptic) and M2 muscarinic receptors (post synaptic).

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6
Q

How does ACh stimulate bronchoconstriction

A

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

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7
Q

How is excessive bronchoconstriction prevented?

A

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

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8
Q

Which neurotransmitter is released by sympathetic nervous system and produces bronchodilation? And which receptors does it bind to?

A

Adrenaline. It binds to the Beta 2 receptors

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9
Q

What is the effect of adrenaline?

A

Adrenaline is a Beta 2 agonist. It stimulates bronchodilation and inhibits histamine secretion from mast cells and mucus secretion. It is an anti-inflammatory

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10
Q

What are NANC dilators? Give 2 examples

A

Non adrenogenic, non cholinergic transmitters released by the Autonomic nervous system that produce vasodilation. examples: NO (nitrous oxide) and VIP

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11
Q

What is the role of sensory nerves?

A

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.

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12
Q

Give examples of inflammatory mediators for constriction of bronchioles

A

histamine, leukotrines, PAF

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13
Q

What are the 4 classes of bronchodilators?

A
  1. Beta 2 antagonists
  2. Muscarinic antagonists
  3. Xanthines
  4. PDE - 4 inhibitors
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14
Q

Name other anti - asthma/anti inflammatory drugs

A

Sodium Cromoglycate
anti inflammatory steroids
Anti - igE
omalizumab

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15
Q

Name 3 Beta 2 antagonists

A
  1. Salbutamol 2. Terbutaline 3. salmeterol (long lasting)
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16
Q

What are the effects of Beta 2 antagonists and how are they taken?

A

Beta 2 antagonists produce bronchodilation and may have an anti-inflammatory role. They are taken in orally for rapid action

17
Q

What are the side effects of beta 2 antagonists and how are they produced?

A
  1. Tachycardia - There are some Beta 2 receptors near the AV node of the heart and the agonists may bind to this
  2. Headache - vasodilation
  3. Tremor - circulating adrenaline
  4. Anxiety - Caused by above 3 symptoms
18
Q

What could happen as a result of taking the Beta 2 agonists orally?

A

They could cause irritation of the respiratory tract and may produce bronchoconstriction as a result

19
Q

What could happen as a result of continuous usage of Beta 2 antagonists?

A

desensitizaiton

20
Q

Which conditions are muscarinic antagonists used for?

A

Chronic obstructive airway disease or intractable asthma

21
Q

Give examples of muscarinic antagonists

A

ipratropium ad oxitropium

22
Q

How can muscarinic antagonists be taken?

A

They are inhaled

23
Q

What is the advantage of muscarinic antagonists and what gives them this quality?

A

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.

24
Q

Give 3 examples of xanthines

A
  1. Caffeine 2. Theophylline 3. Aminophylline
25
Q

When and how are xanthines taken?

A

Xanthines are taken orally for prophylaxis - they are only given as prevention therapy - not for acute asthma

26
Q

Are xanthines slow/fast acting?

A

They are slow acting and have a low therapeutic index

27
Q

What is the range of dosage of xanthines? How much xanthines is considered toxic?

A

effective between 10 - 20 mg/litre

toxic >25 mg/litre

28
Q

What are the side effects of xanthines?

A

Nausea, insomnia, convulsions, diuresis, headache and arrythmias

29
Q

What are the two hypothetical mechanisms of xanthines?

A
  1. Inhibition of PDE. PDE stimulates breakdown of cAMP and cAMP increases levels of cGMP which is responsible for bronchoconstriction.
  2. Adenosine leaks out from compounds all the time and can cause bronchoconstriction. So xanthines inhibit adenosine receptors.
30
Q

Give an example of PDE - 4 inhibitor

A

roflumilast.

31
Q

What is the effect of PDE - 4 inhibitors?

A

They inhibit PDE. PDE stimulates breakdown of cAMP and cAMP increases levels of cGMP which is responsible for bronchoconstriction.

32
Q

How are PDE - 4 inhibitors given?

A

They are given orally

33
Q

What are the side effects of PDE - 4 inhibitors?

A

nausea, vormitting, insomnia, and headache

34
Q

Why are PDE - 4 inhibitors not used?

A

This is because they tend to produce suicidal tendencies in patients

35
Q

Give an example of a leukotrine antagonist?

A

Monteleukast

36
Q

How do Leukotrines antagonists work?

A

Leukotrines are bronchoconstrictors and these antagonists bind to their receptors and inhibit them

37
Q

When and how are leukotrine antagonists taken?

A

They are taken orally and are used in severe asthma or to prevent exercise induced asthma

38
Q

What are the side effects of leukotrine antagonists?

A

Abdominal pain, headache,, respiratory tract infections and suicidal behaviours