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Where are H1 Histamine receptors present?
- Smooth muscle
- Vascular endothelium
- Brain
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Where are H2 Histamine receptors present?
- Gastric parietal cells
- cardiac muscle
- mast cells
- brain
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H1 receptors cause _____ in the lungs, resulting in _____.
- bronchoconstriction
- asthma
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H1 receptors cause _____ in the vascular smooth muscle, resulting in _____.
- post capillary venule dilation
- erythema
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H1 receptors cause _____ in the vascular endothelium, resulting in _____.
- cellular contraction
- edema
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H1 receptors cause _____ in the peripheral nerves, resulting in _____.
- sensitization
- itching, pain
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H2 receptors cause _____ in the heart.
minor increase in HR & contractility
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H2 receptors cause _____ in the stomach, resulting in _____.
- gastric acid secretion
- PUD, GERD
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What kind of drug is an H1-antihistamine?
inverse agonist (stabilizes inactive H1 rc conformation)
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When is Cmax (max plasma concentration) reached with H1-antihistamines?
within 2-3 hours
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How are H1-antihistamines metabolized?
hepatically CYP450
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________ can inhibit arachidonic acid production.
Steroids (glucocorticoids)
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Second gen antihistamine drug names
- Loratadine
- Desloratidine
- Cetirizine
- Levocetirizine
- Fexofenadine
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Two characteristics of second generation H1 antihistamines.
- Lipophilic
- Neutral at physiologic pH
- **Can cross BBB**
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First gen antihistamine drugs.
- Diphenhydramine
- Hydroxyzine
- Chlorpheniramine
- Promethazine
- Doxepin
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Two characteristics of second generation H1 antihistamines.
- Albumin binding
- Ionized at physiologic pH
- **Do not cross BBB**
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Antihistamines are effective in treating?
- Rhinitis, conjunctivitis,
- urticaria, pruritis
- Motion sickness, chemotherapy-related n/v
- Insomnia
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H1 antihistamines are not effective for ______ or ________.
- systemic anaphylaxis
- asthma
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Give ______ for anaphylaxis.
epi
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H1-antihistamines given for motion sickness & chemotherapy-related n/v.
- Diphenhydramine
- dimenhydrinate
- meclizine
- promethazine
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H1-antihistamines for insomnia.
- diphenhydramine
- doxylamine (indicated for sleep)
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AE of H1 antihistamines.
- CNS toxicity
- Sedative effects
- Cardiac toxicity: QT interval prolongation,
- Withdrawal of terfinadine and astemizole
- Anticholinergic effects
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When sympathetic NS is stimulated, result in lungs is _____ by agonism of _____ receptors.
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When parasympathetic NS is stimulated, result in lungs is _____ by agonism of _____ receptors.
- bronchoconstriction
- muscarinic (ACh)
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Three classes of bronchodilators used to tx asthma.
- β-agonists
- Anticholinergics
- Methylxanthines
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Epinephrine agonizes what receptors? What are the resulting actions of each?
- B2 (resulting in airway sm muscle relaxation)
- B1 (can cause tachy, palpitations, arrhythmias)
- α (peripheral vasoconstriction)
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Is Epi used for asthma? Why or why not?
NO! Not selective for B2
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Nonselective beta agonists that are not used for asthma.
- Epinephrine (β2, β1, α)
- Isoproterenol (β2, β1)
- Metoproterenol (β2, β1)
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β-agonists used to tx asthma
- Terbutaline, albuterol, pirbuterol, bitolterol - β2
- Levalbuterol (isolated stereoisomer) - β2
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Long-acting β-agonists (LABA).
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Why isn't atropine used for asthma?
- Rapidly absorbed across respiratory epithelium
- Many AEs:
- tachycardia,
- nausea, dry mouth, GI upset
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Two anticholinergics used for asthma (and COPD). Which one is longer acting?
- Ipratropium bromide (bid)
- Tiotropium (longer acting), (q day)
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Which receptor is most important with anticholinergics? Why?
- M3
- Mediates smooth muscle bronchodilation and mucus gland secretion in the airway
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Two methylxanthines.
- Theophylline
- Aminophylline
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MOA of methylxanthines.
- Inhibition of PDE
- Airway smooth muscle - bronchodilation
- Inflammatory cells - anti-inflammatory
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Methylxanthines antagonize which receptors? What effects result?
- adenosine receptors
- Increased ventilation during hypoxia
- Increased endurance of diaphragmatic muscles
- Decreased mast cell release
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How are Methylxanthines metabolized? Why is this important?
- CYP450 1A2
- Narrow TI so potential for DIs
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What induces CYP 1A2?
Cigarette smoking
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AE of methylxanthines.
- n/v/d, ha, irritability, insomnia;
- seizures, brain damage,
- hyperglycemia, hypokalemia, hypotension,
- cardiac arrhythmias, death
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Methylxanthines work in conjunction with _________.
B-agonists
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Anticholinergics are competitive antagonists at _______________ receptors
muscarinic ACh
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___________ increase the production of cAMP --> bronchodilation.
B2 agonists
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__________ inhibits breakdown of cAMP by inhibiting PDE.
Theophyline
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Anti-inflammatory Agents used to tx asthma & COPD.
- Corticosteroids
- Cromolyns
- Leukotriene
- Inhibitors
- Anti-IgE Antibodies
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Corticosteroids upregulate ________ and _________.
- B2 receptors
- anti-inflammatory proteins
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Corticosteroids decrease ________.
pro-inflammatory proteins
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Corticosteroids induce ________ in _______.
apoptosis in inflammatory cells
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AE of corticosteroids.
- osteopenia/osteoporosis
- delayed growth in children
- oropharyngeal candidiasis, hoarseness hyperglycemia
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Inhaled corticosteroids
- Beclomethasone
- Triamcinolone
- Fluticasone (available in combination with salmeterol)
- Budesonide (available in combination with formoterol)
- Flunisolide
- Mometasone
- Ciclesonide
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Cromolyns stabilize _________ and inhibit the release of ________.
- mast cells
- inflammatory mediators
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Indication for cromolyns.
prophylactic therapy for allergic response
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What is nedocromil?
A cromolyn
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Leukotriene Inhibitors.
- Zileuton (beginning of pathway)
- Montelukast (inhibits binding)
- Zafirlukast (inhibits binding)
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What is Omalizumab?
- Anti-IgE Antibody
- (Humanized mouse monoclonal antibody)
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How does Omalizumab work?
- Binds to IgE
- prevents IgE from binding to mast cells (causing degranulation of mast cells)
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How is Omalizumab administered?
subQ q 2-4 weeks
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Drugs for tx of Gout.
- Probenecid
- Allopurinol
- Colchicine
- Prednisone
- NSAIDs
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How does Allopurinol work?
inhibits Xanthine oxidase, preventing formation of Uric Acid
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How does Probenecid work?
facilitates excretion of uric acid
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Indication for colchicine.
- tx of acute gout attack
- prophylactic tx of gout
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How does colchicine affect uric acid levels?
It doesn't!
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Indications for Probenecid.
prophylactic for gout progression
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Decreases urate reabsorption in the proximal tubules
Probenecid
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Why does probenecid lead to a variety of DIs?
- Non-selective blockade of active renal transport of organic acids
- Includes secretion and reabsorption
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Two specific drugs that interact with Probenecid.
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When should Probenecid NOT be initiated?
during an acute attack
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Increase in frequency, duration, and severity of gout attacks may occur during first 6-12 months tx with this drug.
Probenecid
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How can you minimize urate kidney stones with Probenecid?
- Maintain high fluid intake (2 L/day minimum)
- Alkalinize the urine (NaHCO3)
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How does allopurinol work?
inhibits production of uric acid
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_________ is a prodrug converted by xanthine oxidase.
Allopurinol
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What gout med can you give with Colchicine?
Allopurinol
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Drugs to treat acute gout.
- NSAIDS
- Colchicine
- Glucocorticoids
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Drugs to treat chronic gout.
- Allopurinal
- Probenecid
- Sulfinpyrazone
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