Antihistamines & COPD/Asthma Flashcards
Name the second generation H1 antagonists
Loratadine, cetirizine (Zyrtec), fexofenadine
Describe histamine’s involvement in anaphylaxis and local allergic reactions.
Histamine is not really responsible for anaphylaxis, most sx come from other mediators. However histamine IS responsible for local reactions
Describe histamine’s role in the PNS vs CNS.
PNS: an autocoid; causes itch and pain by stimulating primary afferent nerve endings via H1 (& H3)
CNS: a neurotransmitter in they hypothalamus where body regulates arousal/wakefulness, appetite, and body temp via post-synaptic H1 and/or H2
Discuss hsitamine toxicity
Spoiled fish contain bacteria that convert histidine into histamine and can cause severe n/v, headache, flushing & sweating. Suppress this toxicity via H1 receptor blockers
Describe the mechanism of action of cromolyn sodium.
It directly inhibits mast cell degranulation using ion channel blockers
How can cromolyn sodium be administered?
Often as a nasal spray but also as an inhaler and eye drops and must be used 3-4x/day
Why are first generation antihistamines more likely to cause drowsiness?
Because they have BBB penetration and the second generation H1 blockers do not thus fewer CNS side effects in second generation
How are most antihistamines metabolized and excreted?
Metabolized by the liver and excreted via the urine.
*Exception is fexofenadine which is excreted unchanged in the bile
What can inhibit the effects of fexofenadine?
Grapefruit, orange, and apple juice via intestinal OATP1A2 transporter
Discuss the major adverse effects associated with first generation H1 antagonists
CNS sx, sinus tachycardia, antimuscarinic effects (blurry vision, dry eye/mouth, urinary retention), toxicity can result in seriousCNS depression –> death
Describe the mechanism of action of corticosteroids
They inhibit inflammatory gene transcription (i.e. transcription of cytokines, chemokines, adhesion molecules, inflammatory receptors, enzymes, proteins)
Describe the adverse effects associated with high dose ICS/systemic steroids.
Bone resorption, skin thinning, growth retardation
Describe the mechanism of action of B2 adrenergic agonists.
Relax aw smooth muscle via B2 receptors and inhibit release of mast cell mediators (inhibit microvascular leakage and increase mucociliary transport)
Describe the mechanism of action of anticholinergics
They block the effects of ACh released from the vagus nerve onto M3 receptors thus decreasing smooth muscle contraction and mucus secretion (theoretically)
Describe the adverse effects associated with anticholinergics
Dry mouth; caution w/ older men w/ prostate hyperplasia (urinary retention)
