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Flashcards in Respiratory - Respiratory Drugs Deck (10)
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What is the methyxanthine, 

Etamiphylline camsylate

used for in treating respiratory failure?

Etamiphylline camsylate is a methylxanthine, which means it is is PDE III inhibitor. 

PDE III, or phosphodiesterase III, degrades cAMP in vascular & bronchial smooth-muscle cells, where increased cAMP leads to decreased intracellular calcium levels, and therefore vasodilation. PDE III reduces cAMP levels, and therefore leads to vasoconstriction. A PDE III inhibitor such as etamiphylline would relax smooth muscle in arterioles as well as in bronchioles. 

 - Etamiphylline camsylate stimulates central chemoreceptors in medulla, mimicking normal physiological response to too much CO2, for example


- promote respiration in apnoeic newborn or pre- term animals
- reverse respiratory depression after overdose eg. of general anaesthetic


What type of respiratory ailments are treated with opioid-receptor agonists and opioids?

What are they meant to do, and what are some examples?


Opioid-receptor agonists are also known as anti-tussives.

Agonists bind to opioid receptors within the medulla’s cough centre, depressing the cough reflex.

They mimic enkephalins & endorphins, which are natural, endogenous opioid agonists

Negative feedback for irritant receptors in respiratory tract.






What are three classes of drug to treat accumulation of mucous in the respiratory tract? 

1. Mucolytics

2. Expectorants

3. Nasal decongestants


What do mucolytic drugs do, and what are some examples? 

They break up mucus in the airways. 

Bromhexine - makes mucus less viscous so it can move

Dembrexine - causes secretory glands to produce more fluid, watery, serous mucous.


What are expectorants and what are some examples?

They're supposed to make you cough up mucus by irritating mucus membranes & causing increased clearance of mucus. ie., Supposed to help mucociliary mechanism work better, but it isn't proven & as such they are of limited value.

Oral treatments:

- Ipecacuana - root of a flowering plant; also an emetic
- Squill / Scilla (herb)
- Camphor
- Aniseed

- Ammonium chloride - Guaiacol
- Liquorice extract

Inhaled treatments:

Eucalyptus oil - supposed to increase secretion of watery mucus, but not proven


How do nasal decongestants work and what is one example?

They reduce mucus production in upper respiratory tract & in conditions associated with profuse secretion eg., allergic rhinitus in cats

Pseudoephedrine (Sudafed) - indirectly-acting sympathomimetic that causes release of endogenous norepinephrine from presynaptic nerve terminals, resulting in vasoconstriction (constriction of smooth muscles in nasal mucusa & trachea to constrict secretory glands in airways); these act on alpha-1 & alpha-2 adrenoreceptors



What drugs could be used to relieve bronchoconstriction by antagonising action at M3 receptors?

NB M3 cholinergic receptors typically vasoDILATE arterioles in most organs and skeletal muscle as a parasympathetic response, when bound to their natural ligand, Ach. Their vasodilatory activity is achieved via the release of nitric oxide (NO) from endothelial cells. 

HOWEVER, M3 activation by Ach directly on SMOOTH MUSCLE CELLS - include in the bronchioles - results in CONSTRICTION. (Normally, this vasoconstriction effect is overridden by the vasodilatory effect of NO).

M3 receptor antagonists include Atropine & Ipratroprium bromide

Atropine is well-known as an antagonist to the muscle-constricting effects parasympathetic nervous system; it is used also to dilate pupils. As a bronchodilator, it antagonises the muscle-constricting effects of the M3 receptor.

Ipratroprium bromide - can be inhaled

Adverse effects:

- Antagonising the parasympathetic system can cause a lack of motility in the GIT and enable uncontrolled stimulation of the sympathetic system

- Bronchodilators interfere with mucociliary clearance but if inhaled it is ok as it targets lungs


What drugs could be used to relieve bronchoconstriction by agonising action at ß2 receptors?

NB ß2 receptors, when bound to norepinephrine or epinephrine are vasodilatory because they relax smooth muscle, and so they are bronchodilatory as well. 

Sympathomimetics, their binding to ß2 receptors leads to phosphorylation events that reduce Ca++, promoting relaxation of muscle. Just as β2 receptors work in vascular smooth muscle, & OPPOSITE to β1 receptors in cardiac muscle

β2-selective drugs/ agonists:

Clenbuterol -  very good example of a β2 agonist bronchodilator; good for horses & cattle

Terbutaline: cats & dogs

Salbutamol/Salmeterol: for horses via inhalation

Non-selective beta agonists:

epinephrine (adrenaline) - for emergency treatment - isoprenaline


What are the adverse effects of using ß2 adrenergic receptor agonists or non-selective ß-receptor agonists to treat bronchconstriction?

Since agonists of any ß adrenergic receptor would be a sympathomimetic -- ie., mimicking norepinephrine or epinephrine -- it is possible that these drugs could also bind to other adrenergic receptors to cause very different effects throughout the body. 

For example, the use of clenbuterol, a ß2 sympathomimetic, could also lead to hypotension due to too much vasodilation of coronary & skeletal-muscle arterioles, which could also experience muscle tremors.

A non-selective sympathomimetic could bind to ß1receptors, causing tachycardia.

Hypokalaemia (increased metabolism of potassium by liver) 


What classes of drugs could be used to treat airway inflammation?

Inflammation can be treated with

1. Glucocorticoids - NSAIDs: aspirin, naproxen

2. Methylaxanthines - etamiphylline

3. Histamine (H1) antagonists (antihistamines)

4. 5-HT aka seratonin antagonists

5. leukotriene (LT) D4- receptor antagonists

6. (Prophylactic) sodium cromoglycate & medocromil sodium

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