Pharmacology Flashcards

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1
Q

<p>What conditions can be exaberated with use of cholinomimetric agents?</p>

A

<p>COPD</p>

<p>Asthma</p>

<p>Peptic ulcers</p>

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2
Q

<p>What is the function of Bethanechol and what type of activity <strong>(nicotinic/muscarinic)</strong>does it have?</p>

A

<p><strong>Function:</strong>Activates the bladder (smooth muscle)</p>

<p><strong>Activity:</strong>Muscarinic</p>

<p><strong>NOTE:</strong>Bethanechol is resistant to AChE</p>

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3
Q

<p>Bethanechol should be prescribed in cases of \_\_\_\_\_\_\_\_.</p>

A

<p>Urinary retention</p>

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4
Q

<p>List the direct agonists of AChE.</p>

A

<p>Bethanechol</p>

<p>Carbachol</p>

<p>Methacholine</p>

<p>Pilocarpine</p>

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5
Q

<p>Which class of receptor are muscarinic receptors?</p>

A

<p>G- protein</p>

<p><b>NOTE:</b>M1= Gq; M2= Gi; M3= Gq</p>

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6
Q

<p>What is the major function of M1 (muscarinic) receptors?</p>

A

<p>Mediates higher cognitive functions, stimulates enteric nervous system</p>

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7
Q

<p>What is the major function of M2(muscarinic) receptors?</p>

A

<p>Decrease heart rate and cotnractility of<strong>atria</strong></p>

<p><strong>REMEMBER:</strong>M2 receptors are only present on the atria and the SA and AV nodes</p>

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8
Q

<p>What is the major function of M3 (muscarinic) receptors?</p>

A

<ul>
<li>Increase exocrine gland secretions</li>
<li>Increase gut peristalsis</li>
<li>Increase bladder contraction, bronchoconstriction</li>
<li>Increase pupillary sphincter muscle contration, ciliary muscle contraction (accommodation)</li>
<li>Increase insulin release, endothelium-mediated vasodilation</li>
</ul>

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9
Q

<p>What is the function of carbochol?</p>

A

<p>Constricts pupil and relieves intraocular pressure in open-angle glaucoma</p>

<p><strong>NOTE:</strong>Carbochol has both nicotinic and muscarinic activity</p>

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10
Q

<p>Metacholine acts as a challenge test for diagnosis of \_\_\_\_\_\_\_\_\_.</p>

A

<p>Asthma</p>

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11
Q

<p>What is the function of methacholine?</p>

A

<p>Stimulates muscarinic receptors in airway when inhaled</p>

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12
Q

<p>Which direct cholinomimetric agents are resistant to AChE?</p>

A

<p>Bethanechol</p>

<p>Carbochol</p>

<p>Pilocarpine</p>

<p></p>

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13
Q

<p>What is the function of pilocarpine?</p>

A

<ul>
<li>Contracts ciliary muscle of eye, pupillary sphincter</li>
</ul>

<p><strong>NOTE:</strong>Contraction of ciliary muscle treats<strong>open-angle glaucoma</strong>and contraction of pupillary sphincter treats<strong>closed- angle glaucoma</strong></p>

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14
Q

<p>Of the 4 direct acetylcholine agonists, which can cross the blood-brain barrier?</p>

A

<p>Pilocarpine</p>

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15
Q

<p>In what cases is pilocarpine administered?</p>

A

<ul>
<li>Open-angled glaucoma</li>
<li>Close-angled glaucoma</li>
<li>Xerostomia (Sjogren syndrome)</li>
</ul>

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16
Q

<p>What is the G-protein class for each of the sympathetic receptors?</p>

A

<p><strong>a1-</strong>q</p>

<p><strong>a2-</strong>i</p>

<p><strong>B1-</strong>s</p>

<p><strong>B2-</strong>s</p>

<p><strong>B3-</strong>s</p>

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17
Q

<p>What are the major functions of a1 receptors?</p>

A

<ul>
<li>Increase vascular smooth muscle contraction</li>
<li>Increase pupillary dilator muscle contraction (mydriasis)</li>
<li>Increase intestinal and bladder sphincter muscle contraction</li>
<li></li>
</ul>

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18
Q

<p>What are the major functions of a2receptors?</p>

A

<ul>
<li>Decrease in sympathetic (adrenergic) outflow</li>
<li>Decrease in insulin release</li>
<li>Decrease in lipolysis</li>
<li>Increase in platelet aggregation</li>
<li>Decrease in aqueous humor production</li>
</ul>

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19
Q

<p>What are the major functions of B1receptors?</p>

A

<ul>
<li>Increase in heart rate</li>
<li>Increase in contractility</li>
<li>Increase in renin release</li>
<li>Increase in lipolysis</li>
</ul>

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20
Q

<p>What are the major functions of B2receptors?</p>

A

<ul>
<li>Vasodilation</li>
<li>Bronchodilation</li>
<li>Increase lipolysis</li>
<li>Increase insulin release</li>
<li>Increase glycogenolysis</li>
<li>Decrease in uterine tone (tocolysis)</li>
<li>Increase in aqueous humor production</li>
<li>Increase in cellular K+ uptake</li>
</ul>

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21
Q

<p>What are the major functions of B3receptors?</p>

A

<ul>
<li>Increase in lipolysis</li>
<li>Increase in thermogenesis in skeletal muscle</li>
<li>Increase in bladder relaxation</li>
</ul>

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22
Q

<p>What is the mechanism of action of Gq class proteins?</p>

A

<p>1. Phospholipase is activated by aGq receptor</p>

<p>2.<strong>Phospholipase C</strong>converts PIP2 to DAG and IP3</p>

<p>3.<strong>IP3</strong>then diffuses through the cytosol to bind toIP3receptors, particularlycalcium channelsin thesmooth endoplasmic reticulum(ER).</p>

<ul>
<li>This causes the cytosolic concentration of <strong>calcium to increase</strong>, causing a cascade of intracellular changes and activity.</li>
</ul>

<p>4. Ca2+ acts with DAG to produce <strong>p</strong><strong>rotein kinase C</strong></p>

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23
Q

<p>Which receptors are of the Gq protein class?</p>

A

<p>H1 (Histamine)</p>

<p>a1 (sympathetic)</p>

<p>V1 (vasopressin)</p>

<p>M1 (muscarinic)</p>

<p>M3 (Muscarinic)</p>

<p><strong>MNEMONIC:</strong>Have 1 M &amp;M</p>

<p><strong>NOTE:</strong>Receptors in the Gq protein class stimulate<strong>smooth muscle contraction</strong></p>

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24
Q

<p>What is the mechanism of action of Gs receptors?</p>

A

<p>1. Gs receptors stimulate adenyl cyclase</p>

<p>2. Adenyl cyclase converts ATP into<strong>cAMP</strong></p>

<p>3. cAMP activates<strong>protein kinase A</strong></p>

<ul>
<li>Sequesters Ca2+ in sarcoplasmic reticulum (heart)</li>
<li>Inhibits myosin light-chain kinase (smooth muscle)</li>
</ul>

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25
Q

<p>Which receptors are on the Gs protein class?</p>

A

<p>B1</p>

<p>B2</p>

<p>B3</p>

<p>D1</p>

<p>H2</p>

<p>V2</p>

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26
Q

<p>What is the mechanism of action for Gi receptors?</p>

A

<p>Gi inhibits Adenylyl cyclase</p>

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27
Q

<p>Which receptors are of the Gi protein class?</p>

A

<p>M2 (muscarinic)</p>

<p>a2 (sympathetic)</p>

<p>D2 (Dopamine)</p>

<p><strong>MNEMONIC:</strong>People who are<strong>2 MAD</strong>inhibit themselves</p>

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28
Q

<p>When should albuterol be administered? What about salmeterol?</p>

A

<p><strong>A</strong>lbuterol=<strong>A</strong>cute asthma/COPD</p>

<p><strong>S</strong>almeterol=<strong>S</strong>erial (long- term) asthma<strong>/</strong>COPD</p>

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29
Q

<p>Which direct sympathomimetics have both B2 and B1 action with the B2 action being greater than the B1 action?</p>

A

<p>Albuterol</p>

<p>Salmeterol</p>

<p>Terbutaline</p>

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30
Q

<p>When should terbutaline be administered?</p>

A

<p>Acute bronchospasm in asthma and tocolysis (inhibition of uterine contractions)</p>

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31
Q

<p>Which sympathomimetic only has a1 action?</p>

A

<p>Midodrine</p>

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32
Q

<p>When should midodrine be administered?</p>

A

<p>In cases of autonomic insufficiency and postural hypotension</p>

<p><strong>NOTE:</strong>Midodrine may exacerbate supine hypertension</p>

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33
Q

<p>What is the mode of action of isoproterenol?</p>

A

<p>B1=B2</p>

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34
Q

<p>When should isoproterenol be administered?</p>

A

<p>Electrophysiologic evaluation of tachyarrythmias</p>

<p><strong>NOTE:</strong>Isoproterenol can worsen ischemia</p>

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35
Q

<p>What is the mode of action of epinephrine?</p>

A

<p>B>a</p>

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36
Q

<p>What is the mode of action of norepinephrine?</p>

A

<p>a1>a2>B1</p>

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37
Q

<p>What is the mode of action for phenylephrine?</p>

A

<p>a1>a2</p>

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38
Q

<p>When should epinephrine be administered?</p>

A

<ul>
<li>Anaphylaxis</li>
<li>Asthma</li>
<li>Open-angle glaucoma</li>
</ul>

<p><b>NOTE:</b>The alpha effect predominates at <u>low</u>doses</p>

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39
Q

<p>What is the mode of action of dobutamine?</p>

A

<p>B1>B2, a</p>

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40
Q

<p>When should dobutamine be administered?</p>

A

<ul>
<li>Heart failure</li>
<li>Cardiogenic shock (inotropic> chronotropic)</li>
<li>Cardiac stress testing</li>
</ul>

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41
Q

<p>When should norepinephrine be administered?</p>

A

<ul>
<li>Hypotension</li>
<li>Septic shock</li>
</ul>

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42
Q

<p>When should phenylephrine be administered?</p>

A

<ul>
<li>Hypotension (vasoconstrictor)</li>
<li>Ocular procedures (mydriatic)</li>
<li>Rhinitis (decongestant)</li>
<li>Ischemic priapism</li>
</ul>

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43
Q

<p>Which drugs are anticholinesterases (indirect agonist)?</p>

A

<p>Donepezil</p>

<p>Rivastigmine</p>

<p>Galantamine</p>

<p>Edrophonium</p>

<p>Neostigmine</p>

<p>Physostigmine</p>

<p>Pyridostigmine</p>

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44
Q

<p>Which anticholinesterases are first line for Alzheimer's disease?</p>

A

<p>Donepezil</p>

<p>Rivastigmine</p>

<p>Galantamine</p>

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45
Q

<p>What is the function of edrophonium?</p>

A

<p>Used to diagnose myasthenia gravis 0.0</p>

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<p>Used to diagnose myasthenia gravis</p>

<p><strong>NOTE:</strong>This has been replaced by anti-AChR Ab (anti-acetylcholine receptor antibody) test</p>

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46
Q

<p>Which of the anitcholinesterases cannot cross the CNS?</p>

A

<p>Neostigmine</p>

<p>Pyridostigmine</p>

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47
Q

<p>When should neostigmine be administered?</p>

A

<ul>
<li>Postoperative and neurogenic ileus (muscles of your intestines stop contracting) and urinary retention</li>
<li>Myastenia gravis</li>
<li>Reversal of neuromuscular junction blockage (postoperative)</li>
</ul>

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48
Q

<p>What is the function of physostigmine?</p>

A

<p>Antidote for anticholinergic toxicity</p>

<p><strong>NOTE:</strong>Physostigmine can freely cross the blood-brain barrier</p>

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49
Q

<p>Which drugs are used along side pyridostigmine to control its side effects?</p>

A

<p>Glycopyrrolate</p>

<p>Hyoscyamine</p>

<p>Propantheline</p>

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50
Q

<p>What is the function of pyridostigmine?</p>

A

<ul>
<li>Treats myasthenia gravis (long term)</li>
<li>Increases muscle strength</li>
</ul>

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51
Q

<p>What is the primary cause of anticholinesterase poisoning?</p>

A

<p><strong>Organophosphates</strong>that irreversibly inhibit AChE</p>

<p>NOTE: Organophosphates are commonly used as insecticides and as a result anticholinesterase poisoning</p>

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52
Q

<p>What are the muscarinic effects of anticholinesterase poisoning?</p>

A

<ul>
<li>Diarrhea</li>
<li>Urination</li>
<li>Miosis</li>
<li>Bronchospasm</li>
<li>Bradycardia</li>
<li>Emesis</li>
<li>Lacrimation</li>
<li>Sweating</li>
<li>Salivation</li>
</ul>

<p><strong>MNEUMONIC:</strong><strong>DUMBBELLS</strong></p>

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53
Q

<p>Muscarinic effects caused by anticholinesterase poisoning can be reversed by \_\_\_\_\_\_\_\_\_\_\_\_.</p>

A

<p><strong>Atropine</strong></p>

<p><strong>NOTE:</strong>Atroprine acts as a competitive inhibitor and can cross the BBB to relieve CNSsymptoms</p>

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54
Q

<p>What are the nicotinic effects of anticholinesterase poisoning?</p>

A

<p>Neuromuscluar blockage</p>

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55
Q

<p>Nicotinic effects of anticholinesterase are reversed by \_\_\_\_\_\_\_\_.</p>

A

<p><strong>Pralidoxime</strong>, which regenerates AChE if given early</p>

<p><strong>NOTE:</strong>Pralidoxime does not readily cross the BBB</p>

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56
Q

<p>What are the CNS effects of anticholinesterase poisoning?</p>

A

<p>Respiratory depression</p>

<p>Lethargy</p>

<p>Seizures</p>

<p>Coma</p>

<p></p>

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57
Q

<p>What are the muscurinic antagonists? Which organ systems are affected?</p>

A

<p><strong><u>Eye</u></strong></p>

<ul>
<li>Atropine</li>
<li>Homatropine</li>
<li>Tropicamide</li>
</ul>

<p><strong><u>CNS</u></strong></p>

<ul>
<li>Benztropine</li>
<li>Trihexyphenidyl</li>
<li>Scopolamine</li>
</ul>

<p><strong><u>GI, Respiratory</u></strong></p>

<ul>
<li>Glycopyrrolate</li>
</ul>

<p><strong><u>GI</u></strong></p>

<ul>
<li>Hyoscyamine</li>
<li>Dicyclomine</li>
</ul>

<p><b><u>Respiratory</u></b></p>

<ul>
<li>Intratropium</li>
<li>Tiotropium</li>
</ul>

<p><b><u>Genitourinary</u></b></p>

<ul>
<li>Oxybutaynin</li>
<li>Solifenacin</li>
<li>Tolterodine</li>
</ul>

58
Q

<p>What muscarinic antagonists affect the eye? What is theirfunction?</p>

A

<p><strong>Antagonists:</strong>Atropine, Homatropine, Tropicamide</p>

<p><strong>Function:</strong>Produces mydriasis (dilation of pupil and cycloplegia (paralysis of ciliary muscle)</p>

<p></p>

59
Q

<p>What muscarinic antagonists affect the CNS? What is the function of each?</p>

A

<p><strong>Antagonists:</strong>Benztropine, trihexyphenidyl</p>

<ul>
<li><b>Function:</b>Treats Parkinson disease and acute dystonia</li>
</ul>

<p><strong>Antagonists:</strong>Scopolamine</p>

<ul>
<li><strong>Function:</strong>Motion sickness</li>
</ul>

<p></p>

60
Q

<p>Which muscarinic antagonists affect the GI and respiratory system?</p>

A

<p><strong>Antagonists:</strong>Glycopyrrolate</p>

<ul>
<li><strong>Function</strong>

<ul>
<li><strong>​Nonoral:</strong>Preoperative uste to reduce airways secretion</li>
<li><strong>Oral:</strong>Drooling, peptic ulcers</li>
</ul>
</li>
</ul>

61
Q

<p>Which muscarinic antagonists affect the GI system?</p>

A

<p><strong>Antagonists:</strong>Hyoscyamine, dicyclomine</p>

<ul>
<li><b>Function:</b>Antispasmodics for irritable bowel syndrome</li>
</ul>

62
Q

<p>Which muscarinic antagonists affect therespiratory system?</p>

A

<p><strong>Antagonist:</strong>Ipratropium, tiotropium</p>

<ul>
<li><strong>Function:</strong>COPD, asthma</li>
</ul>

63
Q

<p>Which muscarinic antagonists affect the genitourinarysystem?</p>

A

<p><strong>Antagonist:</strong>Oxybutynin, solifenacin, tolterodine</p>

<ul>
<li><strong>Function:</strong>Reduce bladder spasms and urge urinary incontinence (overactive bladder)</li>
</ul>

64
Q

<p>What affect does atropine have on the following systems?</p>

<p><strong>Eye</strong></p>

<p><strong>Airway</strong></p>

<p><strong>Stomach</strong></p>

<p><strong>Gut </strong></p>

<p><strong>Bladder</strong></p>

A

<p><strong>Eye</strong></p>

<ul>
<li>Increases pupil dilation</li>
<li>Cycloplegia</li>
</ul>

<p><strong>Airway</strong></p>

<ul>
<li>Bronchodilation</li>
<li>Decrease in secretions</li>
</ul>

<p><strong>Stomach</strong></p>

<ul>
<li>Decrease acid secretion</li>
</ul>

<p><strong>Gut </strong></p>

<ul>
<li>Decrease motility</li>
</ul>

<p><strong>Bladder</strong></p>

<ul>
<li><strong>​</strong>Decrease urgency in cystitis</li>
</ul>

<p><strong>NOTE:</strong>Atropine reduces the effects (<strong>DUMBELLS)</strong>of anticholinesterases, but not the nicotinic effects</p>

65
Q

<p>What are the adverse effects of atropine?</p>

A

<ul>
<li>Increase in body temp (due to decrease in sweating)</li>
<li>Increase in HR</li>
<li>Dry mouth</li>
<li>Dry, flushed skin</li>
<li>Cyclopegia</li>
<li>Constipation</li>
<li>Disorientation</li>
</ul>

<p><strong>MNEUMONIC</strong>: Hot as a hare, dry as a bone, red as beet, blind as a bat, mad as a hatter, full as a flask</p>

<p><strong>NOTE:</strong>Can cause acute angle-closure glaucoma in in <strong>elderly</strong>(due to mydriasis),<strong>urinary retention</strong>in men with prostatic hyperplasia, and hyperthermia in <strong>infants</strong></p>

66
Q

<p>\_\_\_\_\_ is inversely related to the affinity of the enzyme for its substrate.</p>

A

<p>Km</p>

67
Q

<p>\_\_\_\_\_\_ is directly propertional to the enzyme concentration.</p>

A

<p>Vmax</p>

68
Q

<p>What affect do competitive inhibitors have on Vmax, Km, and pharmocodynamics?</p>

A

<p><strong>Vmax:</strong>Unchanged</p>

<p><strong>Km:</strong>Increased</p>

<p><strong>Pharmocodynamics:</strong>Decrease potency</p>

69
Q

<p>What affect do irreversible competitive inhibitors have on Vmax, Km, and pharmocodynamics?</p>

A

<p><strong>Vmax:</strong>Decrease</p>

<p><strong>Km:</strong>Unchanged</p>

<p><strong>Pharmocodynamics:</strong>Decrease in efficacy</p>

70
Q

<p>What affect do noncompetitive inhibitors have on Vmax, Km, and pharmocodynamics?</p>

A

<p><strong>Vmax:</strong>Decrease</p>

<p><strong>Km</strong>: Unchanged</p>

<p><strong>Pharmacodynamics:</strong>Decrease efficacy</p>

71
Q

<p>What is bioavailabilty (F)?</p>

A

<p>Fraction of administered drug reaching systemic circulation unchanged</p>

<p><strong>NOTE:</strong>IV, F=100%; Oral. F<100% due to incomplete absorption and first pass metabolism</p>

72
Q

<p>Vd</p>

A

<p>Theoretical volume occupied by the total amount of drug in the body relative to its plasma concentration</p>

<p>Vd= (amount of drug in the body)/ (plasma drug concentration)</p>

<p></p>

73
Q

<p>The apparent volume distribution of drug can be altered by \_\_\_\_\_\_ and \_\_\_\_\_\_\_ disease.</p>

A

<p>Liver; kidney</p>

<p><b>NOTE:</b>Protein binding will decrease, so Vd will increase.</p>

74
Q

<p>When is Vd low?</p>

A

<p>When a high percentage of drug is bound to plasma proteins.</p>

<p><b>Ex:</b>Plasma/ intravascular</p>

75
Q

<p>When is Vd high?</p>

A

<p>When a high percentage of a drug is being sequestered in tissues.</p>

<p><strong>NOTE:</strong>This raises the possibility of displacement by other agents .</p>

76
Q

<p>Clearance</p>

A

<p>The volume of plasma cleared of drug per unit time.</p>

<p><strong>NOTE:</strong>Clearance may be imparied with defects in cardiac, hepatic, or renal function</p>

<p>CL= (rate of elimination of drug)/ (plasma drug concentration); CL= Vd X Ke (elimination constant)</p>

77
Q

<p>Half- life</p>

A

<p>The time required to change the amount of drug in the body by 1/2 during elimination.</p>

<p>t1/2= (0.7 X Vd)/ CL</p>

<p><strong>NOTE:</strong>Time to steady state depends primarily on t1/2and is independent of dose and dosing frequency.</p>

78
Q

<p>In \_\_\_\_\_\_\_\_\_ kinetics, a drug infused at a constant rate takes 4-5 half-lives to reach steady state.</p>

A

<p>First order kinetics</p>

<p><strong>NOTE:</strong>It takes 3.3 half-lives to reach 90 % of the steady state level</p>

79
Q

<p>Loading dose</p>

A

<p>(CpX Vd)/ (F)</p>

<p>Cp= target plasma concentration at steady state</p>

<p><strong>NOTE:</strong>In renal disease, maintenance dose is decreased and loading dose is usually<u>unchanged</u>.</p>

80
Q

<p>Maintenance dose</p>

A

<p>(CpX CL xT)/ (F)</p>

<p>Cp= target plasma concentration</p>

<p>T= dosage interval (time between doses), if not administered continuously</p>

<p><strong>NOTE:</strong>In renal or liver disease, maintence dose decreases and loading dose is usually unchanged.</p>

81
Q

<p>Additive drug interactions</p>

A

<p>Effect of substance A and B together is equal to the sum of their individual effects</p>

<p><b>EX:</b>Aspirin and acetaminophen</p>

82
Q

<p>Permissive drug interactions</p>

A

<p>Presnce of substance A is required for the full effects of substance B</p>

<p><strong>EX:</strong>Cortisol on catecholamine responsiveness</p>

83
Q

<p>Synergestic drug interactions</p>

A

<p>Effect of substance A and B together is greater than the sum of their individual effects</p>

<p><strong>EX:</strong>Clopidogrel with aspirin</p>

84
Q

<p>Tachyphylactic drug interactions</p>

A

<p>Acute decrease in response to a drug after initial/ repeated administration</p>

<p><strong>EX:</strong>Nitrates, niacin, pheylephrine, LSD, MDMA</p>

85
Q

<p>What effect does a competitive antagonist have on potency and efficacy?</p>

A

<p><strong>Potency:</strong> Decrease</p>

<p><strong>Efficacy:</strong>No change</p>

<p><strong>NOTE:</strong>A competitive antagonist can be overcome by increasing the agonist concentration.</p>

<p><strong>EX:Diazepram</strong> (agonist) +<strong>flumazenil</strong>(competitive antagonist) on GABAAreceptor</p>

86
Q

<p>What effect does a noncompetitive antagonist have on potency and efficacy?</p>

A

<p><strong>Potency:</strong>Decrease</p>

<p><strong>Efficacy:</strong>Decrease</p>

<p><strong>NOTE:</strong>A noncompetitive antagonist cannot be overcome by increasing agonist concentration</p>

<p><strong>EX:</strong>Norepinephrine (agonist) + phenoxybenzamine (noncompetitive antagonist) on a- receptors</p>

87
Q

<p>Zero-order elimination</p>

A

<p>Rate of elimination is<strong>constant</strong>regardless of Cp. Cpdecreases linearly with time.<strong>Capacity-limited elimination</strong></p>

<p><strong>EX:</strong>Phenytoin, Ethanol, and Aspirin (at high or toxic concentrations)</p>

88
Q

<p>First-order elimination</p>

A

<p>Rate of first-order elimination is<strong>directly proportional</strong>to the drug concentration.<strong>Flow-dependent elimination</strong></p>

<p><strong>NOTE:</strong>Cpdecreases exponentially with time</p>

<p>*Applies to<u>most</u>drugs</p>

89
Q

<p>Which drugs eliminate via zero-order elimination?</p>

A

<p>Phenytoin, Ethanol, and Aspirin</p>

90
Q

<p>How is TCA toxicity generally treated?</p>

A

<p>With sodium bicarbonate to overcome the sodium channel-blocking activity of TCAs</p>

<p><strong>NOTE:</strong>This is not true in cases of accelerating drug elimination</p>

91
Q

<p>Phase I Drug metabolism</p>

A

<p><strong>Reduction, Oxidation, Hydrolysis</strong>with<strong>cytochrome P-450</strong>usually yield slightly polar, water-soluble metabolites, which are often still active</p>

<p><strong>NOTE:</strong>Geriatric patients lose phase I first</p>

92
Q

<p>Phase II</p>

A

<p>Conjugation (<strong>methylation, glucuronidation, acetylation, sulfation</strong>) usually yields very polar, inactive metabolites, which are renally excreted.</p>

<p><strong>NOTE:</strong>Patients who are slow acetylators have increase side effects from certain drugs, because a decrease rate of metbolism.</p>

93
Q

<p>What is the therapeutic window?</p>

A

<p>Dosage range that can safely and effectively treat disease</p>

94
Q

<p>Therapeutic index</p>

A

<p>T50/ ED50</p>

<p>(Median toxic dose)/ (Median effective dose)</p>

<p><strong>NOTE:</strong>Safer drugs have higher TI values. Drugs with lower TI values frequently require monitoring</p>

<p><strong>EX:</strong>Warfarin, Theophylline, Digoxin</p>

95
Q

<p>\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ are part of the sympathetic pathway but are innervated by cholinergic fibers.</p>

A

<p>Sweat glands</p>

96
Q

<p>Where are NNreceptors found?</p>

A

<p>Autonomic ganglia</p>

<p>Adrenal medulla</p>

97
Q
A
98
Q

<p>Where are NMfound?</p>

A

<p>Neuromuscular junction of skeletal muscle</p>

99
Q

<p>What are the clinical applications of amphetamine?</p>

A

<p>Narcolepsy, obesity, ADHD</p>

100
Q

<p>Indirect sympathomimetics</p>

A

<p>Amphetamine</p>

<p>Cocaine</p>

<p>Ephedrine</p>

101
Q

<p>Characteristics of amphetamine</p>

A

<p>Indirect general agonist</p>

<p>Reuptake inhibitor</p>

<p>Releases stored catecholamines</p>

102
Q

<p>What are effects of cocaine?</p>

A

<p>Causes<strong>vasoconstriction</strong>and<strong>local anesthesia</strong></p>

<p><strong>NOTE:</strong>Caution when giving B-blockers if cocaine intoxication is suspected (can lead to unopposed a1activation, which can lead to extreme hypertension and coronary vasospasm)</p>

103
Q

<p>Characteristics of cocaine</p>

A

<p>Indirect general agonist</p>

<p>Reuptake inhibitor</p>

104
Q

<p>Characteristics of ephedrine</p>

A

<p>Indirect general agonist</p>

<p>Releases stored catechlamines</p>

105
Q

<p>What are the clinical applications of ephedrine?</p>

A

<p>Nasal decongestion (pseudoephedrine)</p>

<p>Urinary incontinence</p>

<p>Hypotension</p>

106
Q

<p>How do norepinephrine and isoproterenol differ?</p>

A

<p><strong>Norepinephrine</strong></p>

<ul>
<li>Increases systolic and diastolic pressures as a result of a1mediated vasoconstriction</li>
<li>Increases mean arterial pressure</li>
<li>Reflex bradycardia</li>
</ul>

<p><strong>Isoproterenol</strong></p>

<ul>
<li>​B2mediated vasodilation</li>
<li>Decrease in mean arterial pressure</li>
<li>Increase in heart rate throughB1and reflex activity</li>
</ul>

107
Q

<p>List a2agonistsTiza</p>

A

<p>Clonidine</p>

<p>Guanfacine</p>

<p>a-methydopa</p>

<p>Tizanidine</p>

<p></p>

108
Q

<p>What are the clinical applications of clonidine?</p>

A

<ul>
<li>Hypertensive urgency (limited situations)</li>
<li>ADHD</li>
<li>Tourette syndrome</li>
<li>Symptom control in opoid withdrawl</li>
</ul>

109
Q

<p>What are the clinical applications of guanfacine?</p>

A

<p>Hypertensive urgency (limited situations)</p>

<p>ADHD</p>

<p>Tourette syndrome</p>

<p>Symptom control in opoid withdrawl</p>

110
Q

<p>What are the adverse effects of clonidine?</p>

A

<ul>
<li>CNS depression</li>
<li>Bradycardia</li>
<li>Hypotension</li>
<li>Respiratory depression</li>
<li>Miosis</li>
<li>Rebound hypertension with abrupt cessation</li>
</ul>

111
Q

<p>What are the clinical applications of a-methyldopa?</p>

A

<p>Hypertension in pregnancy</p>

112
Q

<p>What are the adverse effects of a-methyldopa?</p>

A

<ul>
<li>Positive direct Coombs hemolysis</li>
<li>Drug-induced lupus</li>
</ul>

113
Q

<p>What is the clinical application for tizanidine?</p>

A

<p>Relief of spasticity</p>

114
Q

<p>What are the adverse effects of tizanidine?</p>

A

<p>Hypotension</p>

<p>Weakness</p>

<p>Xerostomia (dry mouth)</p>

115
Q

<p>List the nonselective a-blockers</p>

A

<ul>
<li>Phenoxybenzamine</li>
<li>Phentolamine</li>
</ul>

116
Q

<p>What are the clinical applications of phenoxybenzamine?</p>

A

<p><strong>Pheochromocytoma</strong>(used preoperatively) to prevent hypertensive (catecholamine) crisis</p>

<p><strong>NOTE:</strong>Phenoxybenzamine is an<u>irreversible</u>nonselective a-blocker</p>

117
Q

<p>What is the clinical application of phentolamine?</p>

A

<p>Given to patients of MAO inhibitors who eat tyramine-containing foods and for severe cocaine induced hypertension (2nd line)</p>

118
Q

<p>What are the irreversible effects of phentolamine?</p>

A

<ul>
<li>Orthostatic hypotension</li>
<li>Reflex tachycardia</li>
</ul>

119
Q

<p>List the a1selective blockers?</p>

A

<p>Prazosin</p>

<p>Terazosin</p>

<p>Tamsulosin</p>

<p><strong>NOTE:</strong>They all have an -osin ending</p>

120
Q

<p>What are the adverse effects of a1selective blockers?</p>

A

<ul>
<li>1st-dose orthostatic hypotension</li>
<li>Dizziness</li>
<li>Headache</li>
</ul>

121
Q

<p>What are the a2selective blockers?</p>

A

<p>Mirtazapine</p>

122
Q

<p>What are the clinical applications of mirtazapine?</p>

A

<p>Depression</p>

123
Q

<p>What are the adverse effects of mirtazapine?</p>

A

<ul>
<li>Sedation</li>
<li>Increase in serum cholesterol</li>
<li>Increase in appetite</li>
</ul>

124
Q

<p>What response does epinephrine have to mirtazapine?</p>

A

<p>Epinephrine response exhibits<strong> reversal of mean arterial pressure</strong> from a net increase to a net decrease (theB2effect)</p>

125
Q

<p>What response does phenylephrine have to mirtazapine?</p>

A

<p>Response is supressed</p>

126
Q

<p>List B1selective blockers</p>

A

<ul>
<li>Acebutolol (partial agonist)</li>
<li>Atenolol</li>
<li>Betaxolol</li>
<li>Bisoprolol</li>
<li>Esmolol</li>
<li>Metoprolol</li>
</ul>

127
Q

<p>List nonselective B blockers</p>

A

<ul>
<li>Nadolol</li>
<li>Pindolol (partial agonist)</li>
<li>Propranolol</li>
<li>Timolol</li>
</ul>

128
Q

<p>List drugs that act as both a and B blockers</p>

A

<p>Carvedilol</p>

<p>Labetalol</p>

129
Q

<p>\_\_\_\_\_\_\_\_\_\_\_\_\_ combines cardiac-selective B1- adrenergic blockage with stimulation of B3receptors.</p>

A

<p>Nebivolol</p>

130
Q

<p>What is the clinical application of timolol?</p>

A

<p>Decrease production of aqueous humor, to treat glaucoma</p>

131
Q

<p>Which B-blockers treat heart failure?</p>

A

<ul>
<li>Bisoprolol</li>
<li>Carvedilol</li>
<li>Metoprolol</li>
</ul>

<p><strong>NOTE:</strong>They act by decreasing motality</p>

132
Q

<p>What is the clinical application of propranolol?</p>

A

<p>Control symptoms of <strong>hyperthyroidism</strong></p>

<ul>
<li>Decrease heart rate</li>
<li>Decrease tremor</li>
</ul>

133
Q

<p>Which B-blockers treat supraventricular tachycardia?</p>

A

<p>Metroprolol, esmolol</p>

<p><strong>NOTE:</strong>They act by decreasing AV conduction velocity (classantiarrhythmic)</p>

134
Q

<p>Which B-blockers treat variceal bleeding?</p>

A

<p>Nadolol, propranolol, carvedilol</p>

<p><strong>NOTE:</strong>They act by decreasing hepatic venous pressure gradient and portal hypertension</p>

135
Q

<p>B-blockers are administered for which conditions?</p>

A

<ul>
<li>Angina pectoris</li>
<li>Glaucoma</li>
<li>Heart failure</li>
<li>Hypertension</li>
<li>Hyperthyroidism</li>
<li>Hypertrophic cardiomyopathy</li>
<li>Myocardial infarction</li>
<li>Supraventricular tachycardia</li>
<li>Variceal bleeding</li>
</ul>

136
Q

<p>How do B-blockers act to treat angina pectoris?</p>

A

<ul>
<li>Decrease heart rate and contractility, resulting in decrease in O2consumption</li>
</ul>

137
Q

<p>How do B-blockers act to treat hypertension?</p>

A

<ul>
<li>Decrease cardiac output</li>
<li>Decrease renin secretion (due to B1-receptor blockade on JG cells)</li>
</ul>

138
Q

<p>How do B-blockers act to treeat hypertrophic cardiomyopathy?</p>

A

<ul>
<li>Decrease heart rate</li>
<li>Increase filling time, relieving obstruction</li>
</ul>

139
Q

<p>How do B-blockers act to treat myocardial infarction?</p>

A

<ul>
<li>Decrease O2demand (short-term)</li>
<li>Decrease mortality (long-term)</li>
</ul>

140
Q

<p>What are the adverse effects of B-blockers?</p>

A

<ul>
<li>Erectile dysfunction</li>
<li>Cardiovascular (bradycardia, AV block, HF)</li>
<li>CNS (seizures, sleep alterations)</li>
<li>Dyslipidemia</li>
<li>Asthma/ COPD exacerbations</li>
</ul>

141
Q

<p>\_\_\_\_\_\_\_\_\_\_\_\_ (insulin/glucagon) treats B-blocker toxicity.</p>

A

<p>Glucagon</p>