The quizzes about Respiratory System Pharmacology: Asthma and COPD

I. Start the exam by click the “Start” button

Respiratory System Pharmacology: Asthma and COPD

Please wait while the activity loads.
If this activity does not load, try refreshing your browser. Also, this page requires javascript. Please visit using a browser with javascript enabled.

If loading fails, click here to try again

Start

Congratulations - you have completed Respiratory System Pharmacology: Asthma and COPD. You scored %%SCORE%% out of %%TOTAL%%. Your performance has been rated as %%RATING%%

Your answers are highlighted below.

Question 1

A 27-year-old patient i s seen in the outpatient cl inic for a routine checkup. She’s just moved to your town, and this i s the fi rst time you’ve met She has asthma and says she’s been using her inhaler (albuterol) most days each week (sometimes twice a day) as her only therapy. “I breathe a lot easier after I take several puffs,” she says. She feels well otherwise. Which statement applies to this patient or her treatment plan?

A	Her treatment plan i s inappropriate and needs to be modified
B	If pulmonary function tests performed at your hospital today are normal, i t i s l ikely that the diagnosis i s incorrect: she does not have asthma
C	She i s l ikely to enjoy activities, such as skiing and skating, in which she breathes cold, clear air
D	She i s most l ikely to have trouble with her breathing when in a warm, humid atmosphere
E	She i s probably s l ightly bradycardic and hypertensive from the drug’s expected actions on the heart and peripheral vasculature

Question 1 Explanation:

This patient certainly seems to have recurrent episodes of asthma. Even if they are “mild” and ostensibly responsive to an inhaled β2 agonist, she’s not being treated properly. She or her prior prescriber has been overreliant on, and overusing, a medication that only manages symptoms (and not well in her case) and does not address the underlying cause, which is airway inflammation. (Some physicians define overuse of an inhaled adrenergic bronchodilator more than once a day; the NIH says needing to use it more than twice a week is overuse.) Reasonable options for her would be to prescribe an inhaled corticosteroid (beclomethasone, others), since she reports only mild symptoms. (Of course, pulmonary function tests [PFTs] should be done.) If her bouts become more severe or frequent, then an oral steroid (eg, prednisone) might be prescribed for a while, with a proper switch to an inhaled steroid. The PFTs might be reasonably normal (b), but that depends on such factors as when she used her inhaler last, and whether she is simply having a “good day” (eg, no exposure today to allergens, etc). A single normal PFT in a patient who describes frequent need for a bronchodilator does not rule out asthma. Let’s use an analogy that applies to many asthma patients. You are standing right on the edge of a thousand-foot drop-off on the rim of the Grand Canyon. Only a couple of inches from a bad trip down. Take just one little step forward and you’re a goner. Same with asthma: you may be “feeling good” with current medications, but just a little provocation of airway inflammation and bronchoconstriction and severe symptoms, possibly necessitating intubation or leading to a fatal attack, can put the patient over the proverbial edge. Patients with asthma tend not to do well in cold temperatures (c). Breathing cold air often provokes bronchospasm (probably mediated by increased parasympathetic effects on airway smooth muscle). (Have you ever taken a deep breath when the temperatures are near or below zero?) Conversely, asthmatics tend to do well when it is warm and humid. (Ever noticed how many athletes with asthma tend to gravitate to sports that provide a warm, humid environment, eg, swimming?) Finally, β2 agonists do not cause bradycardia or increases of peripheral resistance. Muscarinic agonists or β-blockers would cause the former, α agonists the latter.

Question 2

Certain adrenergic agonists clearly play a role in managing some patients with asthma, whether for prophylaxis (control medication) or for rescue Which drug i s classified as an adrenergic agonist, but has no physiologically relevant or cl inically useful effects on airway smooth muscle tone?

A	Albuterol
B	Epinephrine
C	Norepinephrine
D	Salmeterol
E	Terbutaline
F	Theophylline

Question 2 Explanation:

Recall that “adrenergic bronchodilation” requires activation of β2-adrenergic receptors on airway smooth muscle cells. Norepinephrine is an α and β1 agonist, with no ability to activate β2 receptors, and so it has no bronchodilator activity. Albuterol (a), a β2 agonist, can be considered the prototype of rapidly acting adrenergic bronchodilators used for asthma (prophylaxis/control, but mainly rescue therapy). Epinephrine (b) is a very efficacious bronchodilator, but its use for routine management of asthma is considerably limited due to its ability to cause vasoconstriction (α-agonist activity) and cardiac stimulation (β1 agonist activity). In terms of pulmonary problems, it is reserved mainly for managing anaphylaxis or status asthmaticus, but it indeed causes bronchodilation well and promptly. Salmeterol (d) is a β agonist also. Given by inhalation, its bronchodilator effects are slow in onset, but it has a long duration compared with similarly classified drugs such as albuterol. Thus, salmeterol is an efficacious bronchodilator, but not suitable for prompt effects (rescue therapy). Terbutaline (c) is classified as a rapidly acting β2 agonist, similar to albuterol. However, it is seldom used any more, whether as an adrenergic bronchodilator or for its other main use as a uterine relaxant to help manage premature labor. Theophylline (f) has modest bronchodilator activity, but it is not an adrenergic agonist. It inhibits phosphodiesterase, and so inhibits metabolic inactivation of c-AMP (the “second messenger” formed by adrenergic bronchodilators in airway smooth muscle).

Question 3

A patient with asthma has moderate bronchospasm and wheezing about twice a Current medications are inhaled albuterol (mainly for acute symptom control) and inhaled beclomethasone as a “control medication.” The patient continues to have occasional and generally mild flare-ups of his asthma. If the physician wishes to make salmeterol part of the treatment plan, how best should i t be used for this patient?

A	A replacement for the albuterol
B	A replacement for the corticosteroid
C	An add-on to current medications for additional prophylactic benefits
D	Primary (sole) therapy, replacing both albuterol and the steroid
E	The preferred agent for acute symptom control (rescue therapy)

Question 3 Explanation:

If you were to decide to use salmeterol in this situation, it would be best to consider it as an add-on. Recall that salmeterol, like albuterol, is mainly a β2 agonist, but salmeterol’s onset of action is much slower, its duration of action much longer. The slow onset of salmeterol makes it a useful prophylactic agent for some patients, but renders it completely inappropriate for rescue therapy (a, e). It can be administered separately, or the physician might prescribe one of the proprietary fixed-dose combination products that contain both salmeterol and a steroid (given by oral inhalation). One could reasonably argue that salmeterol is also dangerous if used as the sole intervention for rescue, because serious ventilatory compromise can develop before its bronchodilator effects develop. The patient described needs a corticosteroid. You might increase the dose of the inhaled steroid as a start, or perhaps try a burst of an oral steroid (eg, prednisone) for a while. Regardless, using salmeterol as a replacement for any corticosteroid (b) or for all the other current medications (d) is likely to provoke more and more severe asthma attacks. Indeed, current guidelines are that if salmeterol or another long-acting β agonist is used, it must be used as an adjunct to a corticosteroid. Remember: The key to success in asthma therapy long-term requires controlling airway inflammation, and corticosteroids are the key drugs for doing just that.

Question 4

The attending in the outpatient pulmonary cl inic states she i s going to start omalizumab therapy for a 19-year-old with refractory What most accurately describes the actions, uses, or adverse effects of this drug?

A	Antibody that binds and therefore inactivates endogenous ACh and histamine
B	Contraindicated i f patient i s taking an oral or orally inhaled corticosteroid
C	Good alternative to albuterol or s imilar adrenergic bronchodilators for rescue therapy
D	Immediate- or delayed-onset anaphylactic reactions pose the greatest ri sk
E	Novel agent l ikely to become fi rst-l ine therapy as a control medication for mild but recurrent asthma

Question 4 Explanation:

The most serious adverse response to omalizumab, a monoclonal antibody directed against IgE, is an anaphylactic reaction (often severe, less often fatal). These adverse reactions usually (not always!) occur after the first dose, and usually within 2 hours of injection. This is one reason why patients should receive the drug only in a “controlled” health care setting and should be under observation for at least 2 hours thereafter. Nonetheless, anaphylaxis or less severe untoward immunologic reactions have been reported 24 hours or longer, and so the patient should have an epinephrine autoinjector (self-injector) (prescribed or dispensed by the physician) handy for at least several days after an omalizumab dose. The risk of anaphylaxis is also a major reason why the drug should be used only for patients who have severe asthma not adequately controlled with other drugs (adrenergic bronchodilators, leukotriene receptor blockers, corticosteroids). As noted, the antibody is directed against IgE. The IgE-omalizumab complex then prevents IgE from binding to mast cell and basophil membranes, which otherwise would trigger allergen-mediated cell activation. Omalizumab does not bind other ligands (eg, ACh or histamine; a), nor does it alter the effects of those bronchoconstrictor agonists in any other way. It also has no intrinsic or direct bronchodilator activity. Owing to the anaphylaxis risk, the drug’s slow onset of action, and its lack of bronchodilator activity, omalizumab is not, nor ever will be, firstline therapy for asthma (e), whether mild or severe, frequent or not. It will never be a substitute for a rapidly acting adrenergic bronchodilator for rescue therapy (c). And prior or current use of any of the “traditional” asthma medications does not contraindicate (b) a trial with omalizumab. Indeed, owing to omalizumab’s slow onset, continued and otherwise proper corticosteroid therapy to suppress airway inflammation is essential.

Question 5

A 19-year-old moves from a small town to your ci ty, and i s now your He has a history of asthma, and his previous primary care physician was managing i t with oral theophylline. What best summarizes the efficacy or current status of theophylline in particular, or methylxanthines in general, in such patients as this?

A	Dosing i s s imple and convenient, rarely needs to be adjusted
B	Excellent alternative to an inhaled steroid for “rescue” therapy
C	Is , at best, a second- or third-line agent for long-term asthma control
D	Possesses strong and cl inically useful anti-inflammatory activity
E	Sedation i s a major s ide effect, even with therapeutic doses or blood levels

Question 5 Explanation:

Theophylline, the prototype methylxanthine, is an oral bronchodilator that has some beneficial pulmonary effects in patients with asthma or COPD. We don’t know precisely how it exerts its bronchodilator activity, at least at concentrations found in human beings (in vitro it inhibits phosphodiesterase, preserving cAMP levels; it also blocks receptors for adenosine, which has bronchoconstrictor activity). However, there are serious problems with this old drug that relegate it to second or third status in therapy; that render it a drug that should be prescribed only by pulmonologists who are quite familiar with the limitations, side effects, and toxicity; and that make its use as primary therapy for asthma usually inappropriate (at best).Theophylline (and other methylxanthines) has a very low therapeutic index: it is all too easy (whether because of drug-drug interactions, or simply improper dosing) to have blood levels rise into a range that can cause toxicity (mainly excessive cardiac and CNS stimulation, with the potential for arrhythmias or seizures). Moreover, and because of the problems stated above, frequent blood testing is necessary in order to get, and keep, plasma levels within an acceptable therapeutic range and hopefully avoid subtherapeutic or toxic blood levels. The drug depends on hepatic P450 status for its elimination, and that makes elimination very easily influenced by liver dysfunction or other interacting drugs that can either induce or inhibit its metabolism. Most important is the fact that theophylline has no anti-inflammatory activity; as I said, if we are treating asthma long-term, the “secret to success” is controlling airway inflammation. For our foundation we use corticosteroids to suppress inflammation. If we were dealing with COPD and the goal is bronchodilation (it is), such drugs as ipratropium (inhaled antimuscarinic) are not only more efficacious than a methylxanthine or an adrenergic bronchodilator but also associated with fewer dosing problems, monitoring needs, and side effects. In COPD the pathophysiology involves not only bronchoconstriction but also goblet cell hyperplasia, leading to increased mucus production. Such drugs as ipratropium are, therefore, usually a first choice and usually improve symptoms and pulmonary function tests the most

Question 6

An elderly man with COPD i s being managed with several drugs, one of which i s inhaled What i s the main mechanism that accounts for the beneficial effects of this drug?

A	Blocks receptors upon which an endogenous bronchoconstrictor mediator acts
B	Enhances epinephrine release from the adrenal medulla
C	Inhibits cAMP breakdown via phosphodiesterase inhibition
D	Prevents antigen-antibody reactions that lead to mast cell mediator release
E	Stimulates ventilatory rates (CNS effect in brain’s medulla)

Question 6 Explanation:

You should be able to deduce quickly (if not simply know outright) that ipratropium is an atropine-like drug—an antimuscarinic that blocks the bronchoconstrictor effect of ACh on airway smooth muscle. It is a quaternary, inhaled antimuscarinic: that is, it acts locally in the airways, and very little of the “always charged” molecule diffuses into the circulation to cause systemic effects. Ipratropium has no effects on the adrenal medulla, on mast cells or other elements of the inflammatory response, or in the CNS. Ipratropium is approved for managing COPD, but is often used for some asthma patients. The drug has a rapid onset of action. However, some studies indicate that it is not as efficacious a bronchodilator as β2 agonists, and so it is not a suitable agent for rescue therapy. Finally, the bronchodilator effects of ipratropium and β agonists are synergistic (same effect, different mechanisms), and so there’s some logic to using them both.

Question 7

A 16-year-old girl treated for asthma develops drug-induced skeletal muscle tremors. What was the most l ikely cause?

A	Albuterol
B	Beclomethasone
C	Cromolyn
D	Ipratropium
E	Montelukast

Question 7 Explanation:

Of the drugs listed in the question, skeletal muscle tremor is a side effect most often associated with β2-adrenergic agonists—albuterol and others. It is almost always a dose-dependent phenomenon. (Note: Some physicians titrate the dose of adrenergic bronchodilators upward, stopping when tremors develop and equating the blood level associated with that dose as being therapeutic with respect to controlling the pulmonary disease. The wisdom of that is questionable; proper dosage adjustments or other therapy changes should be based on pulmonary symptom relief [subjective assessment] in general and, ideally, quantitative pulmonary function tests.) None of the other drugs listed is associated with skeletal muscle tremor. Beclomethasone (b) is an inhaled corticosteroid; cromolyn (c), also inhaled for asthma, reduces mast cell degranulation; ipratropium (d) is an inhaled antimuscarinic indicated for COPD; montelukast (e) is a leukotriene receptor blocker that is also indicated for asthma prophylaxis.

Question 8

A 26-year-old patient with asthma i s being treated with montelukast. What i s the main mechanism by which this drug works?

A	Blocks receptors for certain proinflammatory and bronchoconstrictor arachidonic acid metabolites
B	Enhances release of epinephrine from the adrenal (suprarenal) medulla
C	Increases airway β-adrenergic receptor responsiveness to endogenous norepinephrine
D	Inhibits cAMP breakdown via phosphodiesterase inhibition
E	Prevents antigen-antibody reactions that lead to mast cell mediator release
F	Stimulates ventilatory rates (CNS effect in brain’s medulla)

Question 8 Explanation:

Montelukast (and a related drug, zafirlukast) blocks receptors for leukotrienes (LTs). (When you see “leuk” or “luk” as part of these drugs’ generic names, think leukotrienes or leukotriene modifiers, and think of drugs for asthma.) Recall that the LTs are proinflammatory and bronchoconstrictor mediators formed as part of normal arachidonic acid metabolism via the 5′- lipoxygenase pathway. LTs also participate in recruiting eosinophils to the inflamed regions (recall that local eosinophilia is often an accompaniment of asthma), thereby blunting the local inflammatory processes in yet another way. In the context of asthma therapy leukotriene receptor blockers are indicated for prophylaxis (control therapy) only, and should not be used in lieu of corticosteroids (oral or orally inhaled) when corticosteroids are suitable (which is most of the time). They will do virtually no good in a short enough time if they were administered to suppress ongoing bronchoconstriction (eg, for rescue therapy), mainly because they are too slowacting. It’s worth noting that although montelukast works well as a control medication for many asthma patients, it is not a panacea. For about 50% of asthma patients its efficacy appears to be no better than placebo. The leukotriene modifiers do not enhance epinephrine release from the adrenal medulla (b), increase β-adrenergic receptor responsiveness (c; note that norepinephrine, mentioned in the question, has no bronchodilator activity because it is not a β2 agonist), inhibit phosphodiesterase (d), or interfere with mast cell function or mast cell responsiveness to antigens (e). Note: Remember the two other main classes of drugs that affect either the formation or breakdown of arachidonic acid. The cyclooxygenase pathway(s) metabolize arachidonic acid to form various prostaglandins, prostacyclin (PGI2), and thromboxanes (eg, thromboxane A2). The cyclooxygenases are inhibited by the traditional nonsteroidal anti-inflammatory drugs, of which aspirin is a reasonable and common example. The (gluco) corticosteroids work “upstream” of both lipoxygenase and cyclooxygenase. They inhibit the formation of arachidonic acid by inhibiting phospholipase activity, which thereby removes substrate for both lipoxygenase and cyclooxygenase metabolism

Question 9

An elderly man, in obvious respiratory distress due to exacerbation of his emphysema and chronic bronchitis (COPD), presents in the emergency One drug ordered by the physician, to be administered by the respiratory therapist, i s N-acetylcysteine. What i s the main action or purpose of this drug?

A	Blocks receptors for the cysteinyl leukotrienes
B	Inhibits metabolic inactivation of epinephrine or β2 agonists that were administered
C	Inhibits leukotriene synthesis
D	Promptly suppresses airway inflammation
E	Reverses ACh-mediated bronchoconstriction
F	Thins airway mucus secretions for easier removal by suctioning or postural drainage

Question 9 Explanation:

You should know N-acetylcysteine as an antidote for acetaminophen poisoning. When used for that purpose, it is given orally or intravenously. The sulfhydryl groups that are part of the molecule are important, as they react with the toxic acetaminophen metabolite and spare glutathione-depleted hepatocytes from oxidative attack. N-Acetylcysteine is also a mucolytic (mucusthinning) drug, given by inhalation in a nebulized solution or by intratracheal instillation, to reduce the viscosity of airway mucus that can then be removed easier by coughing, postural drainage and chest percussion, or airway suctioning. Here, too, the mechanism is based on its -SH-rich composition. N-Acetylcysteine lacks other airway effects such as bronchodilation or suppression or inflammation.

Question 10

A 23-year-old woman with asthma has what i s described as “aspirin (hyper)sensitivity” (triad asthma) and experiences severe bronchospasm in response to even small doses of the What i s the most l ikely mechanism by which the aspirin provoked her pulmonary problems?

A	Blocked synthesis of endogenous prostaglandins that have bronchodilator activity
B	Induced formation of antibodies directed against the salicylate on airway mast cells
C	Induced hypersensitivity of H1 receptors on airway smooth muscles
D	Induced hypersensitivity of muscarinic receptors on airway smooth muscles
E	Prevented epinephrine binding to β2-adrenergic receptors (airways and elsewhere)

Question 10 Explanation:

Aspirin, the prototype of the nonsteroidal anti-inflammatory drugs (NSAIDs), inhibits cyclooxygenases (COX-1 and -2) and the “arachidonic acid cascade.” One outcome of that is inhibited synthesis of PGE2. The PGE2 (along with circulating epinephrine) is a physiologically important endogenous bronchodilator that is particularly important to maintain airway patency (dilation) for most asthmatics. Inhibit this synthesis, with aspirin or another nonselective cyclooxygenase inhibitor/NSAID, and bronchoconstriction or bronchospasm may ensue in that population of asthmatics who often are exquisitely sensitive to these drugs. This aspirin hypersensitivity phenomenon is relatively uncommon in children with asthma, but more prevalent in adults. Estimates are that it affects between 10% and 25% of adult asthmatics with so-called “triad asthma”: asthma plus nasal polyps, chronic urticaria, and the NSAID sensitivity. Virtually all other NSAIDs that nonselectively inhibit COX-1 and -2 may cross-react, although the incidence of severe pulmonary reactions seems the highest with aspirin itself. Selective COX-2 inhibitors (ie, celecoxib) pose less of a problem because they are less likely to inhibit the bronchodilator prostaglandins that are formed by the COX-1 pathway, but they are not absolutely free from the potential problem. If one needs a drug to manage fever or mild pain in an asthmatic, acetaminophen is preferred: it does not cross-react. Owing to negligible effects on prostaglandin synthesis via cyclooxygenase-dependent pathways, it is not classified as an NSAID.

Question 11

A young boy i s diagnosed with His primary symptom i s frequent cough, not bronchospasm or wheezing. Other asthma medications are started, but until their effects develop fully we wish to suppress the cough without running a ri sk of suppressing ventilatory drive or causing sedation or other unwanted effects. Which drug would meet these needs the best?

A	Codeine
B	Dextromethorphan
C	Diphenhydramine
D	Hydrocodone
E	Promethazine

Question 11 Explanation:

Dextromethorphan is a centrally acting antitussive drug that is about as efficacious a coughsuppressant as codeine. It is thought to suppress the vagal afferent neural pathway involved in the cough reflex. However, unlike codeine (c) and hydrocodone (d; another useful antitussive in some cases), dextromethorphan is not an opioid and lacks analgesic effects or the potential for ventilatory suppression or abuse. Diphenhydramine (c) and promethazine (e) also have antitussive action. However, they, too, can cause generalized CNS and ventilatory depression. They also exert significant antimuscarinic effects, but neither is a preferred or even frequently used drug for cough suppression in most patients, and in asthma patients in general. Although the atropine-like effects of these drugs may be beneficial in terms of inhibiting AChmediated bronchoconstriction in a patient with asthma, they may also cause thickening of airway mucus, favoring plugging of the airways with viscous mucus deposits that cannot be removed normally by mucociliary transport or by coughing. That is, the benefits of bronchodilation may be outweighed by the risks of mucus plugging in some asthma patients.

Question 12

A mother brings her 10-year-old son, who has a longstanding history of poorly controlled asthma, to the Emergency Department (ED). He i s in a relatively early stage of what will prove to be a severe asthma Arterial blood gases have not been analyzed yet, but i t i s obvious that the lad i s in great distress. He i s panting with great effort at a rate of about 60/min. Given the boy’s history and the l ikely diagnosis of acute asthma, the health care team administers all the drugs l i sted below by the stated routes, and with the purposes noted. The child’s condition quickly improves, and the team leaves the boy with his mother while they go to care for other ED patients. Within a couple of minutes, the mother comes out of her son’s cubicle frantically screaming “he’s stopped breathing!” Which drug most l ikely precipitated the ventilatory arrest?

A	Albuterol, inhaled, given by nebulizer for prompt bronchodilation
B	Atropine, nebulized and inhaled
C	Midazolam, IV, to normalize ventilatory rate and allay anxiety
D	Methylprednisolone (glucocorticosteroid), IV, for prompt suppression of airway inflammation
E	Normal saline, nebulized and inhaled, to hydrate the airway mucosae

Question 12 Explanation:

Aside from the midazolam, any, if not all, the other drugs listed would be appropriate for this patient. The term asthma derives from a Greek word that means, literally, “to pant.” In severe asthma attacks such as the one described here the hyperpnea precedes the likely development of ventilatory depression and, in some cases, ventilatory arrest. This increased ventilatory rate is essential. It is a sometimes successful yet too often inadequate compensatory physiologic response elicited to increase ventilatory oxygen uptake and eliminate excess CO2 (although it may be insufficient to raise arterial O2 saturation adequately and more than sufficient to induce metabolic alkalosis from excess CO2 loss). Nonetheless, it is a “protective” ventilatory response, and breathing too quickly, even inefficiently, is better than not breathing at all. This leads to an admonition: Never give a drug that can depress ventilation or the normal ventilatory drive to an asthma patient unless he or she has a protected airway and ventilation can be controlled and supported mechanically. IV midazolam (or the IV administration of virtually any other benzodiazepine, or, especially an opioid) will allay anxiety, but will also tend to suppress ventilatory drive and hasten the onset of ventilatory arrest. In the scenario described here, diazepam is the wrong drug to give. Albuterol (a) or a similar β2-agonist bronchodilator, whether given by inhalation or parenterally, would not be expected to worsen the boy’s ventilatory status. They should not be the only drugs relied-on, but they would be appropriate adjunctive treatments, as would be all the rest for the stated purposes. As an important aside, you may recall that atropine (b) and other drugs with antimuscarinic activity have bronchodilator activity, but also tend to make airway mucus secretions more viscous, leading to airway mucus plugging. In the context of this scenario, with the administration of other drugs that I listed, and the availability of airway suctioning devices as needed, the mucus-thickening effects of an antimuscarinic should not be a problem with which we cannot easily deal by way of airway suctioning and the administration of mucus-thinning (mucolytic) drugs. Glucocorticoids (d) and nebulized saline would be valuable, if not essential, adjuncts to this boy’s therapy.

Question 13

You prescribe an orally inhaled corticosteroid for a patient with Previously she was using only a rapidly acting adrenergic bronchodilator for both prophylaxis and treatment of acute attacks. She used the steroid as directed for 5 days, and then stopped taking i t. What i s the most l ikely reason why the patient quit using the drug?

A	Disturbing tachycardia and palpitations occurred
B	Relentless diarrhea developed after just 1 day of using the steroid
C	She experienced l i ttle or no obvious improvement in breathing
D	The drug caused extreme drowsiness that interfered with daytime activities
E	The drug caused her to retain fluid and gain weight

Question 13 Explanation:

It usually takes a couple of weeks of inhaled corticosteroid use “as directed” to suppress airway inflammation, and the resulting bronchoconstriction, well enough that the patient can sense clinical improvement (fewer or milder asthma symptoms). Unless the patient is forewarned about this slow onset, and urged to remain compliant, they are likely to believe the drug is ineffective and therefore not worth taking. Clearly, inhaled corticosteroids do not cause the obvious “rush”—the prompt, dramatic, and unmistakable symptom relief that typically occurs with adrenergic bronchodilators. Nonetheless, given adequate time, the inhaled steroids usually prove to be the key to effective long-term control of asthma. Inhaled corticosteroids act locally; little enters the systemic circulation; such side effects as fluid retention, weight gain (e), and hyperglycemia, which are typical with systemic steroids (eg, prednisone), rarely occur or become problematic. Inhaled steroids do not cause cardiac stimulation (a), diarrhea (b), or drowsiness (d).

Question 14

A patient consumes an excessive dose of theophylline and develops toxicity in response to the What i s the expected s ign, symptom, or other consequence of this overdose?

A	Bradycardia
B	Drowsiness progressing to s leep and then coma
C	Hepatotoxicity
D	Paradoxical bronchospasm
E	Seizures

Question 14 Explanation:

Theophylline, a methylxanthine, is a caffeine-like drug that is becoming outmoded as therapy for asthma in most adolescents and adults. It should probably not be prescribed by any physician other than a pulmonologist who is familiar with the limitations and problems with this class of drugs. A low margin of safety, extreme dependence on adequate liver function (for metabolism), susceptibility to numerous clinically significant drug interactions, and a lack of airway anti-inflammatory activity are among the reasons why. Without proper dosage adjustments and monitoring, it is all too easy, and common, for blood levels to fall into subtherapeutic ranges or, as we see here, into toxic ranges. The earliest signs and symptoms of excess involve CNS stimulation (jitteriness, tremors, difficulty sleeping, anxiety). As blood levels rise, the CNS is increasingly stimulated. Seizures may occur, and when they do, the inability to breathe during the seizures is the main cause of death. Thus, answer b is incorrect. Theophylline tends to cause tachycardia, increases of cardiac contractility, and, potentially, tachyarrhythmias. This occurs mainly because methylxanthines inhibit phosphodiesterase, which normally metabolically inactivates cAMP, the levels of which are increased in smooth and cardiac muscles by β-adrenergic agonists. Bradycardia (a) is not at all likely. Theophylline is not hepatotoxic (c); it does not cause paradoxical broncho-spasm (d), even when plasma levels are very high or truly toxic.

Question 15

Acetylcholinesterase inhibitors, muscarinic agonists such as pilocarpine, and β-blockers are among the drugs used to manage patients with They also share properties that are particularly relevant to patients with asthma. Which statement summarizes best what that relevance i s?

A	Contraindicated, or pose great ri sks, for people with asthma
B	Degranulate mast cells, cause bronchoconstriction
C	Tend to raise intraocular pressure in patients who have both glaucoma and asthma
D	Trigger bronchoconstriction by directly activating H1 histamine receptors on airway smooth muscle cells
E	Useful for acute asthma, not for ambulatory patients

Question 15 Explanation:

By now you should be able to recall the classifications and actions of the drugs listed in this question. Acetylcholinesterase inhibitors and such muscarinic agonists as pilocarpine are sometimes used as topical miotics for managing glaucoma (mainly angle-closure/narrow angle forms of the disease). Certain topical β-blockers are used for open-angle glaucoma, probably working by inhibiting aqueous humor production. However, all these drugs (and others in these classes, used systemically for a host of other common medical conditions) are contraindicated for asthma patients—even if or when they are used topically on the eye(s). An important element in the pathophysiology of asthma is airway smooth-muscle hyperresponsiveness to various bronchoconstrictor stimuli, and muscarinic receptor activation is clearly a phenomenon that leads to often intense bronchoconstriction. You may recall that the choline ester, methacholine, is used to help diagnose asthma when the diagnosis is otherwise questionable. The basis of this “methacholine challenge” centers on the concept of airway hyperreactivity (in this case, to muscarinic agonists) in asthmatics. Very low doses of methacholine are given, by inhalation, while pulmonary function tests are recorded. Asthmatics experience significant (sometimes dangerous) bronchoconstrictor responses to methacholine doses that are far lower than those that would provoke even slight changes in nonasthmatics. Recall that ACh esterase inhibitors cause what amounts to a “buildup” of ACh at the neuroeffector junction, leading to heightened muscarinic receptor activation. These cholinesterase inhibitors, whether used for glaucoma or such other conditions as myasthenia gravis, can have lethal effects in some asthma patients. (Note, too, that cholinesterase inhibitors are found in some insecticides, so there is an extra and significant risk to the asthma patient in agricultural or gardening/lawn care settings.) Muscarinic agonists, whether those used for glaucoma or for stimulating the gut or urinary tract (eg, bethanechol for functional urinary retention), may prove lethal too. Finally, asthmatics tend to be extremely dependent on the bronchodilator actions of circulating epinephrine. Block the β2 receptors that mediate that effect and the outcome can be disastrous. Even the so-called “cardioselective” β-blockers (atenolol, metoprolol) can cause serious problems for some asthmatics. That is because their ability to block β1 receptors is relative and dose-dependent, not absolute: they may pose no pulmonary problems for persons without asthma, but may be deadly in those who do.

Question 16

A patient suffering status asthmaticus presents in the emergency Blood gases reveal severe respiratory acidosis and hypoxia. Even large parenteral doses of a selective β₂ agonist fail to dilate the airways adequately; rather, they cause dangerous degrees of tachycardia. Which pharmacologic intervention or approach i s most l ikely to control the acute symptoms and restore the bronchodilator efficacy of the adrenergic drug?

A	Give a l ipoxygenase inhibitor (eg, montelukast)
B	Give a parenteral corticosteroid
C	Give parenteral diphenhydramine
D	Switch to epinephrine
E	Switch to i soproterenol (β1/β2 agonist)

Question 16 Explanation:

When pulmonary function deteriorates so much that respiratory acidosis ensues (because sufficient amounts of CO2 aren’t being eliminated by ventilation) and severe hypoxia develops (because of inadequate oxygen transfer), acute tolerance (in essence, desensitization) develops to the bronchodilator effects of drugs with β2-agonist activity—all of them. If this point is forgotten, repeated administration of a β2 agonist will lead to increasing degrees of cardiac stimulation (rate, contractility, automaticity, conduction) because under these conditions they lose their selectivity for β2 receptors and also begin activating β1 receptors very effectively. They become isoproterenol-like in their profiles, and isoproterenol (e) will not be efficacious. Even epinephrine (d) won’t work as an efficacious bronchodilator under these conditions, and repeated injections of it will do little more than cause further cardiac stimulation via β1 activation, plus vasoconstriction owing to α-adrenergic receptor activation. Through mechanisms that are not quite clear, administering suitable doses of a parenteral steroid under these conditions of acidosis and hypoxia “restores” a substantial degree of airway responsiveness to β agonists. Giving a steroid (plus oxygen, which helps correct the underlying blood gas and pH changes) is essential. Under these conditions there is little likelihood that the severe and refractory airway problems involve excessive activation of airway leukotriene receptors, and so administering a lipoxygenase inhibitor such as montelukast (a) will be of little value. Giving diphenhydramine (c), even though it blocks the bronchoconstrictor effects of both ACh and histamine, will not do much good for the acute and life-threatening signs and symptoms. Therefore, a parenteral corticosteroid, administration of oxygen, and support of ventilation as needed are most likely to have the best outcome.

Question 17

The FDA has mandated a warning about the increased ri sk of death in asthma patients taking recommended doses of salmeterol (or other s low-/long-acting adrenergic asthma control medications) for too long a period of What i s the most l ikely mechanism or phenomenon by which this fatal adverse response, or other severe airway responses, occur?

A	Anaphylaxis due to gradual formation of antibodies against the drug
B	Hypertensive cris i s
C	Inhibited synthesis, release, and anti-inflammatory actions of endogenous cortisol
D	Plugging of the bronchioles with viscous mucus, due to the drug’s antimuscarinic actions
E	Tolerance of airway smooth muscle cells to the effects of adrenergic bronchodilators

Question 17 Explanation:

Long-term, more or less round-the-clock, exposure of β2-adrenergic receptors to an agonist eventually causes those receptors to lose sensitivity to those very drugs. The loss of responsiveness to usual bronchodilator actions—that is, airway smooth muscle tolerance—affects responses not only to salmeterol or the pharmacokinetically similar drug, formoterol, but also to albuterol or similar rapidly acting adrenergic bronchodilators typically used for rescue therapy. Of course, for most drugs overcoming tolerance and restoring effects to a certain intensity can be achieved by increasing the dose, the dose frequency, or both. This is precisely what asthma patients who are poorly managed do, especially with their rapidly acting rescue inhalers (albuterol, etc): four or more puffs at a time, many times each 24 hours. Thus, the “solution” to the tolerance, higher and more frequent doses, actually becomes the cause. And so the usual outcome of excessive or excessively prolonged adrenergic bronchodilator use is a faster onset and progression of tolerance and a greater degree of tolerance. That is, increasing dose and/or frequency only makes matters worse over the long run. So, patients taking one or two β2 agonists month after month gradually get less and less bronchodilation and symptom relief over time; their breathing difficulty becomes worse, and should severe bronchoconstric-tion occur, usual or even relatively high doses of a rapidly acting (rescue) bronchodilator will fail to work well, if at all. Usually this will be assessed, clinically, by diminishing improvement of forced expiratory volume in 1 second (FEV1) in response to a rapidly acting adrenergic bronchodilator (eg, albuterol). Thus, the patient gets in severe ventilatory distress or may even die. Thus, what might be called “antiasthma” drugs can actually lead to asthma-related fatalities under some conditions. Answer a is incorrect; antibodies against salmeterol or other adrener-gic bronchodilators do not develop. Answer b is not acceptable. Although high doses of a so-called “selective β2 agonist” may increase blood pressure (at high blood levels selectivity for β2 receptors is lost and β1 receptors can be activated, raising blood pressure via increases of both heart rate and left ventricular contractility), a significant rise of pressure is very unlikely; hypertensive crisis will not occur. Salmeterol or other adrenergic broncho-dilators have no direct or major effects on cortisol synthesis, release, or actions (c), nor do they have antimuscarinic effects, whether on mucus viscosity, airway smooth muscle tone, or any other processes mediated by muscarinic (cholinergic) receptors.

Question 18

A hungry 8-year-old i s vis i ting his grandparents’ house and sees grandpa sprinkle some powder from a small foil pack onto his Grandpa smiles and says “Mmmm, tastes good.” The packet contains a theophylline salt that was prescribed for his COPD. Liking applesauce, and thinking the drug packets contain candy, the lad opens the applesauce jar, finds grandpa’s stash of dozens of theophylline packets, and sprinkles on lots of drug before eating the whole thing. Toxicity ensues. What i s this child most l ikely to experience, and do so before anything else s ignificant and untoward develops?

A	Acute urinary retention
B	Bradycardia and hypotension
C	Irri tability, other s igns/symptoms of CNS stimulation, possibly seizures
D	Ischemic stroke from drug-induced platelet aggregation
E	Ventilatory suppression (centrally mediated) leading to respiratory acidosis and apnea

Question 18 Explanation:

Theophylline (or the related drug aminophylline) is classified as a methylxanthine, just like the caffeine and other methylxanthines in your favorite coffee, tea, cola, or chocolates. So to answer this question, simply imagine what is likely to happen if you consumed, say, eight cups of strong caffeinated coffee in a short time. You’re typically wide awake (if not simply “hyper”), tachycardic, urinating (from cardiac-mediated increased renal perfusion and GFR), and tremorous. Methylxanthines are CNS stimulants, not just bronchodilators or cardiac stimulants. In overdoses, irritability or increased alertness and awakeness develop first. As blood levels rise, ultimately seizures occur, and that is one of the major things we would see if this child took a sufficient overdose. Methylxanthines don’t cause urinary retention (a); as noted above, increased GFR will lead to more frequent diuresis. Bradycardia and hypotension (b) are the opposite of what is apt to occur in the cardiovascular system. Methylxanthines induce neither platelet aggregation (they weakly inhibit it via a cAMP-dependent mechanism) nor ischemic stroke because of it. If anything, rises of blood pressure from excessive cardiac stimulation might (rarely) cause hemorrhagic stroke. Methylxanthines, of course, stimulate central ventilatory control mechanisms, tending to cause hyperpnea. (Caffeine has been used as a ventilatory stimulant, mainly in newborns.) That, in turn, would likely cause respiratory alkalosis, not acidosis (e). Apnea is not likely

Once you are finished, click the button below. Any items you have not completed will be marked incorrect. Get Results

There are 18 questions to complete.

←

List

→

Return

Shaded items are complete.

1	2	3	4	5
6	7	8	9	10
11	12	13	14	15
16	17	18	End

Return

II. Preview all questions below

1.A 27-year-old patient i s seen in the outpatient cl inic for a routine checkup. She’s just moved to your town, and this is the first time you’ve met She has asthma and says she’s been using her inhaler (albuterol) most days each week (sometimes twice a day) as her only therapy. “I breathe a lot easier after I take several puffs,” she says. She feels well otherwise. Which statement applies to this patient or her treatment plan?

Her treatment plan i s inappropriate and needs to be modified
If pulmonary function tests performed at your hospital today are normal, i t i s l ikely that the diagnosis i s incorrect: she does not have asthma
She i s l ikely to enjoy activities, such as skiing and skating, in which she breathes cold, clear air
She i s most l ikely to have trouble with her breathing when in a warm, humid atmosphere
She i s probably s l ightly bradycardic and hypertensive from the drug’s expected actions on the heart and peripheral vasculature

2. Certain adrenergic agonists clearly play a role in managing some patients with asthma, whether for prophylaxis (control medication) or for rescue Which drug is classified as an adrenergic agonist, but has no physiologically relevant or cl inically useful effects on airway smooth muscle tone?

Albuterol
Epinephrine
Norepinephrine
Salmeterol Terbutaline
Theophylline

3. A patient with asthma has moderate bronchospasm and wheezing about twice a Current medications are inhaled albuterol (mainly for acute symptom control) and inhaled beclomethasone as a “control medication.” The patient continues to have occasional and generally mild flare-ups of his asthma. If the physician wishes to make salmeterol part of the treatment plan, how best should it be used for this patient?

A replacement for the albuterol
A replacement for the corticosteroid
An add-on to current medications for additional prophylactic benefits
Primary (sole) therapy, replacing both albuterol and the steroid
The preferred agent for acute symptom control (rescue therapy)

4. The attending in the outpatient pulmonary cl inic states she is going to start omalizumab therapy for a 19-year-old with refractory What most accurately describes the actions, uses, or adverse effects of this drug?

Antibody that binds and therefore inactivates endogenous ACh and histamine
Contraindicated i f patient i s taking an oral or orally inhaled corticosteroid
Good alternative to albuterol or s imilar adrenergic bronchodilators for rescue therapy
Immediate- or delayed-onset anaphylactic reactions pose the greatest ri sk
Novel agent l ikely to become fi rst-l ine therapy as a control medication for mild but recurrent asthma

5. A 19-year-old moves from a small town to your ci ty, and is now your He has a history of asthma, and his previous primary care physician was managing i t with oral theophylline. What best summarizes the efficacy or current status of theophylline in particular, or methylxanthines in general, in such patients as this?

Dosing i s s imple and convenient, rarely needs to be adjusted
Excellent alternative to an inhaled steroid for “rescue” therapy
Is , at best, a second- or third-line agent for long-term asthma control
Possesses strong and cl inically useful anti-inflammatory activity
Sedation i s a major s ide effect, even with therapeutic doses or blood levels

6. An elderly man with COPD is being managed with several drugs, one of which is inhaled What is the main mechanism that accounts for the beneficial effects of this drug?

Blocks receptors upon which an endogenous bronchoconstrictor mediator acts
Enhances epinephrine release from the adrenal medulla
Inhibits cAMP breakdown via phosphodiesterase inhibition
Prevents antigen-antibody reactions that lead to mast cell mediator release Stimulates ventilatory rates (CNS effect in brain’s medulla)
Suppresses synthesis and release of inflammatory mediators

7. A 16-year-old girl treated for asthma develops drug-induced skeletal muscle What was the most likely cause?

Albuterol
Beclomethasone
Cromolyn
Ipratropium
Montelukast

8. A 26-year-old patient with asthma is being treated with What is the main mechanism by which this drug works?

Blocks receptors for certain proinflammatory and bronchoconstrictor arachidonic acid metabolites
Enhances release of epinephrine from the adrenal (suprarenal) medulla
Increases airway β-adrenergic receptor responsiveness to endogenous norepinephrine
Inhibits cAMP breakdown via phosphodiesterase inhibition
Prevents antigen-antibody reactions that lead to mast cell mediator release
Stimulates ventilatory rates (CNS effect in brain’s medulla)

9. An elderly man, in obvious respiratory distress due to exacerbation of his emphysema and chronic bronchitis (COPD), presents in the emergency One drug ordered by the physician, to be administered by the respiratory therapist, is N-acetylcysteine. What is the main action or purpose of this drug?

Blocks receptors for the cysteinyl leukotrienes
Inhibits metabolic inactivation of epinephrine or β₂ agonists that were administered
Inhibits leukotriene synthesis
Promptly suppresses airway inflammation Reverses ACh-mediated bronchoconstriction
Thins airway mucus secretions for easier removal by suctioning or postural drainage

10. A 23-year-old woman with asthma has what is described as “aspirin (hyper)sensitivity” (triad asthma) and experiences severe bronchospasm in response to even small doses of the What is the most likely mechanism by which the aspirin provoked her pulmonary problems?

Blocked synthesis of endogenous prostaglandins that have bronchodilator activity
Induced formation of antibodies directed against the salicylate on airway mast cells
Induced hypersensitivity of H₁ receptors on airway smooth muscles
Induced hypersensitivity of muscarinic receptors on airway smooth muscles
Prevented epinephrine binding to β₂-adrenergic receptors (airways and elsewhere)

11. A young boy is diagnosed with His primary symptom is frequent cough, not bronchospasm or wheezing. Other asthma medications are started, but until their effects develop fully we wish to suppress the cough without running a risk of suppressing ventilatory drive or causing sedation or other unwanted effects. Which drug would meet these needs the best?

Codeine
Dextromethorphan
Diphenhydramine
Hydrocodone
Promethazine

12. A mother brings her 10-year-old son, who has a longstanding history of poorly controlled asthma, to the Emergency Department (ED). He is in a relatively early stage of what will prove to be a severe asthma Arterial blood gases have not been analyzed yet, but it is obvious that the lad is in great distress. He is panting with great effort at a rate of about 60/min.

Given the boy’s history and the likely diagnosis of acute asthma, the health care team administers all the drugs listed below by the stated routes, and with the purposes noted. The child’s condition quickly improves, and the team leaves the boy with his mother while they go to care for other ED patients. Within a couple of minutes, the mother comes out of her son’s cubicle frantically screaming “he’s stopped breathing!” Which drug most l ikely precipitated the ventilatory arrest?

Albuterol, inhaled, given by nebulizer for prompt bronchodilation
Atropine, nebulized and inhaled
Midazolam, IV, to normalize ventilatory rate and allay anxiety
Methylprednisolone (glucocorticosteroid), IV, for prompt suppression of airway inflammation
Normal saline, nebulized and inhaled, to hydrate the airway mucosae

13. You prescribe an orally inhaled corticosteroid for a patient with Previously she was using only a rapidly acting adrenergic bronchodilator for both prophylaxis and treatment of acute attacks. She used the steroid as directed for 5 days, and then stopped taking it. What i s the most l ikely reason why the patient quit using the drug?

Disturbing tachycardia and palpitations occurred
Relentless diarrhea developed after just 1 day of using the steroid
She experienced l i ttle or no obvious improvement in breathing
The drug caused extreme drowsiness that interfered with daytime activities
The drug caused her to retain fluid and gain weight

14. A patient consumes an excessive dose of theophylline and develops toxicity in response to the What is the expected sign, symptom, or other consequence of this overdose?

Bradycardia
Drowsiness progressing to s leep and then coma
Hepatotoxicity
Paradoxical bronchospasm
Seizures

15. Acetylcholinesterase inhibitors, muscarinic agonists such as pilocarpine, and β-blockers are among the drugs used to manage patients with They also share properties that are particularly relevant to patients with asthma. Which statement summarizes best what that relevance is?

Contraindicated, or pose great ri sks, for people with asthma
Degranulate mast cells, cause bronchoconstriction
Tend to raise intraocular pressure in patients who have both glaucoma and asthma
Trigger bronchoconstriction by directly activating H₁ histamine receptors on airway smooth muscle cells
Useful for acute asthma, not for ambulatory patients

16. A patient suffering status asthmaticus presents in the emergency Blood gases reveal severe respiratory acidosis and hypoxia. Even large parenteral doses of a selective β₂ agonist fail to dilate the airways adequately; rather, they cause dangerous degrees of tachycardia. Which pharmacologic intervention or approach i s most l ikely to control the acute symptoms and restore the bronchodilator efficacy of the adrenergic drug?

Give a l ipoxygenase inhibitor (eg, montelukast)
Give a parenteral corticosteroid
Give parenteral diphenhydramine
Switch to epinephrine
Switch to i soproterenol (β1/β2 agonist)

17. The FDA has mandated a warning about the increased ri sk of death in asthma patients taking recommended doses of salmeterol (or other s low-/long-acting adrenergic asthma control medications) for too long a period of What i s the most l ikely mechanism or phenomenon by which this fatal adverse response, or other severe airway responses, occur?

Anaphylaxis due to gradual formation of antibodies against the drug
Hypertensive cris i s
Inhibited synthesis, release, and anti-inflammatory actions of endogenous cortisol
Plugging of the bronchioles with viscous mucus, due to the drug’s antimuscarinic actions
Tolerance of airway smooth muscle cells to the effects of adrenergic bronchodilators

18. A hungry 8-year-old i s vis i ting his grandparents’ house and sees grandpa sprinkle some powder from a small foil pack onto his Grandpa smiles and says “Mmmm, tastes good.” The packet contains a theophylline salt that was prescribed for his COPD. Liking applesauce, and thinking the drug packets contain candy, the lad opens the applesauce jar, finds grandpa’s stash of dozens of theophylline packets, and sprinkles on lots of drug before eating the whole thing. Toxicity ensues. What i s this child most l ikely to experience, and do so before anything else s ignificant and untoward develops?

Acute urinary retention
Bradycardia and hypotension
Irri tability, other s igns/symptoms of CNS stimulation, possibly seizures
Ischemic stroke from drug-induced platelet aggregation
Ventilatory suppression (centrally mediated) leading to respiratory acidosis and apnea

The quizzes about Respiratory System Pharmacology: Asthma and COPD

I. Start the exam by click the “Start” button

Respiratory System Pharmacology: Asthma and COPD

II. Preview all questions below

Share this:

Related

The quizzes about Renal System and Diuretic Pharmacology

The quizzes about Autacoids and Anti-inflammatory Drug Pharmacology

You may also like

Leave a Comment Cancel Reply