Send the link below via email or IMCopy
Present to your audienceStart remote presentation
- Invited audience members will follow you as you navigate and present
- People invited to a presentation do not need a Prezi account
- This link expires 10 minutes after you close the presentation
- A maximum of 30 users can follow your presentation
- Learn more about this feature in our knowledge base article
Do you really want to delete this prezi?
Neither you, nor the coeditors you shared it with will be able to recover it again.
Make your likes visible on Facebook?
Connect your Facebook account to Prezi and let your likes appear on your timeline.
You can change this under Settings & Account at any time.
Transcript of Respiratory Pharmacology
Note: Patients should rinse with water after inhalation to limit effects on bone and teeth and deposition on soft tissue
SE: Weakened immune system, increased risk of systemic infections, osteoporosis, and elevated pressure in the eyes
Broken down by CYP450 and effected by CYP450i (ritonavir, ketoconazole, etc)
Used mainly as supplementary to corticosteroids if they do not produce desired effects as a monotherapy
Treats: Severe cases of asthma which does not respond to CS use
SE: Anaphylaxis (result of being a injectable protein to a patient who is very allergy sensitive)
You down with OTCs?
(yeah you know me)
Alternative name: Salbutamol
Alternative uses: Can be used together with ipratropium, Acetylcysteine, pulmozyme to treat CF
Effective for: 4-6 hours
Should NOT be used as a mono therapy. Should be concurrently with a CS (beclometasone or fluticasone) to minimize asthma related deaths.
Should NOT be used to treat acute symptoms
Half Life: 5.5 hours (effective for 12hours)
Difference: Formoterol works faster and is more potent (12ug of formoterol as effective as 50ug of salmeterol)
Advair= Fluticasone + Salmeterol
Symbicort= Budesonide+ Formoterol
Other effects: Positive Inotrope, Positive Chronotrope, Increases BP, Increases Renal Flow, Anti-inflammatory, stimulates the meddullary respiratory center
Treatment of OD: Beta Blockers (B1-blockers)
Competitive nonselective PDEi -> raises cAMP, activates PKA, inhibits TNF-a, inhibits LT
Nonselective adenosine receptor antagonist (Blocks A1, A2, A3 equally)
Mechanism: Nonspecific AChRi ->promotes degrdation of cGMP. Does NOT diffuse into the blood (minimizes systemic side effects), is a quarternary amine (does NOT cross the BBB or cause anticholinergic syndrome)
Mechanism: M3 specific AChRi
Note: NEVER used to treat acute asthma attack