Pharmacology of antihistamines and drugs for the treatment of allergic rhinitis
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| Histamine is produced by | Mast cells, basophils, and paracrine cells, CNS neurotransmitter
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| Histidine is converted to histamine by | Enzyme L-histidine decarboxylase
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| Histamine is stored in granules and released from mast cells when | IgE reacts to cause degranulation
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| How can morphine and tubocurarine cause histamine release? | My stimulating IP3 and DAG which releases Ca+ and stimulates mast cell degranulation
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| Histamine can be inactivated by (2 ways) | 1. Methylation from methyltransferease enzyme or 2. Oxidation from diamine oxidase
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| All histamine receptors are | GCPR
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| Which histamine receptors are involved in allergic reactions? | H1
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| Which histamine receptors are involved in gastric acid production and some allergies? | H2
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| What do H3 receptors do? | Used as a feedback mechanism in the brain to inhibit histamine production and release
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| Antihistamines are agonists for which receptors | H1 or H2
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| 1st generation H1 antihistamines cause | Sedation because they cross the BBB
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| 2nd generation H1 antihistamines are usually preferred because | They do not cross the BBB to cause sedation
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| H1 antihistamines are most effectively when taken | Prophylatically
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| Most antihistamines are metabolized by the | Liver
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| Which two antihistamines are not metabolized by the liver? | Hydroxyzine and ceftrizine
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| First generation antihistamines are often used to treat | Nausea, vertigo and for sedation
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| Meclizine is used for | Motion sickness because it is an anitemetic and non-sedating
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| Which drug is used to treat the symptoms of allergic rhinitis? | Azelastine
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| First line treatment of acute allergies | Antihistamines
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| Antihistamines are used for | Acute allergies that are mediated by mast cell-derived histamine but not continuous exposure
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| Which generation of antihistamines has a longer duration? | 2nd
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| Pseudoephedrine does what | Decongestant (but a mild stimulant), used with antihistamines
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| Leukotriene modifier mechanism | Treats pro-inflammatory mediators
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| Leukotriene modifiers | Zileuton, zafirlukast, montelukast
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| Nasal cromyln does what? | Stabilizes mast cells and mediates pro-inflammatory mediatiors
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| Most effective treatment for moderate to severe AR | Intranasal corticosteroids
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| Intranasal corticosteroids | Fluticasone, triamcinolone, flunisolide, budesonide, mometasone, ciclesonide
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| Patients should start intranasal corticosteroids | One week prior to allergy season
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| Intranasal corticosteroids mechanism of action | Decreased nasal eosinophilia, mast cell numbers, and cytokine expression
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| Intranasal corticosteroid Side effects | Local irritation, dryness, and epitaxis
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| Most effective drug to treat allergic rhinitis | Corticosteroids
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| First generation antihistamine | Diphenhydramine
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| Second generation antihistamines | Loratadine and fexofenadine
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| 2nd generation antihistamine with a short half life | Fexofenadine
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| Does intranasal azelastine cause drowsiness? | Yes
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| What does an acute poisoning with 1st gen antihistamines present as | Anticholinergic toxicity ("dryness")
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| Leukotriene modifier mechanism of action | Competitive inhibitor of cysteinyl leukotrienes for CysLT1 receptor binding to inhibit early and late phases of bronchoconstriction induced by antigen challenge
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| Churg-Strauss syndrome | Allergic granulomatous vasculitis due to leukotriene antagoists/modifiers in patients being withdrawn from glucocoricoid therapy
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| Ipratroprium bromide mechanism of action | blocks the muscarinic acetylcholine receptors in the smooth muscles of the bronchi in the lungs, opening the bronchi, also has anticholinergic effects in the nose to relieve rhinorrhea but not congestion
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| Rhinitis medicoamentosa is due to | Down regulation of the alpha receptors by continual use of phenylephrine
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