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Flashcards in Pharmacology of Respiratatory Deck (18)
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1
Q

What are the 3 main respiratory diseases in this lecture?

A

Affecting conducting zone:
Asthma
Bronchitis

Affecting respiratory zone:
COPD:
Small airways disease
Emphysema

2
Q

What happens when an allergic asthmatic inhales an antigen?

A
Mast cells release histamine when allergen is encountered.
Also released:
- Histamine
- Prostaglandins
- Leukotrienes
- Cytokines 
This leads to...
Bronchoconstriction
Oedema
Mucus secretion
Inflammation
3
Q

Explain the 3 phases of when the lung comes into contact with an allergen

A

Immediate phase:

  • Entirely due to brochospasm
  • Released from allergen triggered mast cells acting on bronchiolar smooth muscle to cause contraction

Delayed phase:
Airway narrowing due mainly to mucosal swelling/oedoma as a result of mediators released from inflammatory cells recruited into airways initiated by events of the immediate phase.

Airway hyper-responsiveness:
Combines effects of bronchospasm on an inflamed oedematous airway that is very sensitive to any inhaled irritant.

4
Q

What are the two main drug types used in pharmacological treatment of asthma?

A

Bronchiodilators
e.g. beta 2 agonists
Muscarinic antagonists

Anti-inflammatory agents
e.g. glucocorticosteriods
Xanthines

5
Q

What are the current treatments used in asthma symptoms?

A
  • Short acting beta 2 agonists e.g. salbutamol
  • Long acting beta 2 agonists e.g. Salmeterol
  • Theophylline
6
Q

What does increasing the carbon chain do to a drug?

A

Increases bioavailability.

7
Q

How does a beta-agonist work on a cell?

A

It activated adenylyl cylase which changes ATP to cAMP. Phosphodiesterase then decreases the amount of cAMP which decreases activation of protein kinase A. This leads to muscle relaxation.

8
Q

What does a beta 2 adrenoreceptor agonist do to a cell?

A

Smooths muscles relaxation and inhibits mast cell degradation.
It is administered via the inhaled route (metered dose inhaler, dry powder and nebulizer). May use a nebuliser if someone finds it difficult to breathe in and press the inhaled at the same time.

•Side effects include; tremor, increased heart rate, hypokalemia (targeting beta-receptors at extra-pulmonary sites)

9
Q

What are the effects of muscarinic antagonists on a cell?

A

Prevents smooth muscle contraction and mucus secretion induced by activation of parasympathetic nerves.

Bronchoconstriction is inhibited by muscarinic antagonists e.g. ipatropium bromide and tiotropium bromide.

Mainly used in COPD treatment.

Side effects include dry mouth, constipation, urinary retention.

10
Q

How does a muscarinic antagonist work on a cell?

A

Acetlycholine binds to sodium channels and passing on the impulse (works by inhibiting the nerve pathway).
It deactivates M3 receptors.

11
Q

How do glucocorticosteriods work in asthma?

A

They move through the plasma membrane and associates with a steroid receptor in the cytoplasm. Steroid engages etc receptor and the protein on the receptor dissociates and allows the steroid to enter the nucleus.

12
Q

What are the actions of glucocorticosteriods in asthma?

A
  • Inhibition of leukotriene and cytokine synthesis/release
  • Inhibit recruitment of inflammatory cells (e.g. T cells,eosinophils, mast cells) recruitment
  • Anti-oedema
  • Increases beta-adrenoceptor function (enhances bronchodilator effect of beta2-agonists)
13
Q

What is the role of ICS in asthma therapy?

A
  • Prevents infiltration and activation of inflammatory cells
  • Reduces mucosal oedema
  • Improves airway and hence lung function
  • Decrease airway hyper-responsiveness
  • Reduce symptoms
  • Reduce frequency and severity of exacerbations
14
Q

Side affects of glucocorticosteriods

A
Inhaled route (e.g. fluticasone proprionate)
oral candidiasis (fungal infection)  
hoarseness, cough, voice problems

Oral or prolonged high dose (e.g. prednisolone)
• Growth retardation, bruising
• Suppression of hypothalamic-pituitary axis
• Osteoporosis (serum osteocalcin), water retention (also binds to mineralcorticosteroid receptor), diabetes
Hypertension, weight gain, ocular hypertension

15
Q

Summary on anti-leukotriene drugs

A

Leukotriene receptor antagonist
Relatively long acting (great benefit in severe asthma, orally bioavailable)
Side effects - rare, headache and GI disturbance

16
Q

How do Xanthines work?

A

These are phosphodiesterase inhibitors which then increase cAMP as this enzyme breaks down cAMP.
This means more PKA is activated and phosphorylation will occur leading to relaxation of the bronchioles.

Numerous drug-drug interactions which increase/decrease plasma levels.
Smoking promotes plasma clearance.

17
Q

What do cromones do?

A

Mast cell stabilises.
Reduce inflammatory cells activation and recruitment.
Not as effective as glucocorticosteroids.

18
Q

What does Omalizmab do?

A

Binds to free IgE.
Must be given as an injection.
Very costly.

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