A AND R PHARM ASSIGNMENT 3 Answers & rationales (A&R) for Assignment 3, Pharmacology in Nursing Practice

1. What is true of hypnotics? a. Mechanisms of action include suppression of the reticular activating system that controls wakefulness in our brains. b. Nursing implications include warning against an adverse effect of zolpidem in which some patients sleep-walk and perform activities that are not remembered the next morning. c. The effect of benzodiazepines in the motor cortex helps to relax muscles, thus helping with sleep. d. All the above. 2. The phrase “start low, go slow” can apply to , because . a. titration of pain medications for the elderly : the diminished function of liver and kidneys increase risk of drug toxicity. b. instructions for patients weaning off of chronic opioid use : if they try to stop cold turkey it will be immediately life-threatening. Withdrawal from opioids is very distressing and often painful, but not life-threatening. (On the other hand, withdrawal from alcohol can be indeed life-threatening, resulting in seizures and death if not managed correctly, usually with use of a benzo like lorazepam). c. narcotic abuse definition : it shows that even if you slowly begin opioid use, it can cause your life to become “low” because of high risk of addiction. d. use of adjuvant medications : they should only be used by themselves and not with any other analgesic. This is the opposite from what “adjuvant” means. Examples of adjuvant drugs are, say, use of non-pain-med-related drugs in addition to pain meds… A person with chronic neuropathic pain often benefits from use of an opioid med PLUS an extra medication like an antidepressant. The antidepressant would in this context be called the adjuvant med. 3. A patient has been admitted after overdosing on acetaminophen (Tylenol), with a total ingested dose of 14 g over a period of 1 hour. The patient’s nurse will expect a. lab results showing a high serum creatinine level, indicating renal failure. Much more likely to see S&S of liver failure, not renal failure… see answer D. b. joint pain and hyperuricemia, indicating rapid onset of gout. Joint pain and hyperuricemia are S&S of gout, but have no relevance to what the question is asking. c. agitation and anxiety, since this drug blocks reuptake of adrenergic neurotransmitters from neural synapses. Not the mechanism of action for acetaminophen. d. lab results showing high liver enzyme levels, indicating hepatic failure. Acetaminophen is notorious for causing liver problems when taken in large amounts either over a long period of time or in one lump amount, as in this case. We really don’t want people taking more than 4gms a day, preferably much less. Labs that measure liver enzymes in the blood, such as AST and ALT are checked, and if the enzymes are high, that means hepatocyte destruction is occurring & releasing enzymes into the blood. 4. The patient in the previous question will likely receive as an antidote a. naloxone (Narcan) since it blocks the acetaminophen molecules from attaching to opioid receptor sites. Naloxone is important in blocking opioid receptors in the body, thus used when there is opioid overdose (know the name of this drug well, not only for a test, but for the future when you are giving opioids to your patients and may need to give a reversal.) b. acetylcysteine (Mucomyst) since it increases glutathione, a substance which enhances the ability of the liver cells to metabolize acetaminophen molecules. c. flumazenil (Romazicon) since it increases GABA, a substance which is important in CYP450 enzymatic function. flumazenil is the reversal agent for benzodiazepine overdose… important drug to know, like naloxone, but it doesn’t apply to this question. Also, GABA’s calming effect is enhanced by benzos, not by benzo-blocker like flumazenil. d. midalozam (Versed), a benzodiazepine which will decrease the patient’s agitation and allow the liver to clear the acetaminophen molecules more quickly. Does this sentence make sense to you, based on your readings? Hopefully not. An example of needing to read an answer really closely and realizing that even though it may sound kind of credible, the statement has no factual basis. 5. An RN is speaking to an addiction-cessation group about ways to decrease or stop their addictive substance. Which instructions by the nurse are correct? a. The best way to use a nicotine patch is a step-wise progression of increasing dosage. No —the progression is in decreasing dosages. Often someone with an addiction is encouraged to cut down a little at a time. For instance, if I wanted to lessen my ice cream addiction, I would maybe decrease it by one scoop a day.  b. Chewing nicotine gum will rapidly, temporarily relieve a craving for a tobacco product. The dose goes straight to the blood stream via the highly vascular mucous membranes, just like when a person takes a sublingual medication like nitroglycerin. c. Disulfiram (Antabuse) creates acetaldehyde syndrome and is the best first-line drug for treating DT’s (delirium tremens) in an alcoholic. Disulfiram will create an unpleasant reaction when drinking alcohol, thus it is a preventive. The treatment for DTs would be something that will stop the risk of seizure, so a benzodiazepine such as Ativan is first- line. d. The opioid agonist naltrexone (Revia) is a good treatment for alcohol craving. Revia is a good alcohol-craving treatment for some patients, but it is not an opioid agonist—it is an opioid antagonist. Read answers closely. 6. Massage therapy is ordered as adjunct treatment for a patient with musculoskeletal pain. The patient asks the nurse how “rubbing my muscles” will help the pain go away. The nurse’s response is based on the knowledge that massaging muscles a. decreases the inflammatory response that initiates the painful stimuli. Massage won’t actually decrease inflammation. b. activates large sensory nerve fibers (A fibers) that send signals to the spinal cord to close the gate, thus blocking painful stimuli from reaching the brain. The gate theory of pain transmission is explained in your book in a simplified fashion, and we’ll keep it simple! Very simplistically, we are going to associate A fibers with inhibition of pain. when stimulated, as in massage, they help to alleviate pain (6th edition: see page 156, 3rd paragraph. 7th edition: pg 144 first paragraph ) c. activates small sensory nerve fibers (C fibers) that send signals to the spinal cord to open the gate and allow endorphins to reach the muscles and relieve the pain. C fibers = sensing of pain, so they are associated with being able to assess and feel pain. This is an important part of the protective aspect of pain, but not a good thing when it comes to wanting pain relief. The functioning of these fibers is more often associated with chronic pain issues, whereas A fibers are associated with “normal,” short-lived, acute pain. d. enhances the effect of Substance P, which is an endogenous pain-relieving biochemical modulator. Always associate Substance P with PAIN. It is a neurotransmitter whose presence is associated with feeling pain, not pain-relief. (See articles cited in RRD). 7. Joe Hardy, RN, is about to give a dose of hydromorphone (Dilaudid) to his patient, Ms Umbridge. What does this entail? a. Understanding that as a powerful hypnotic, this drug blocks GABA sites in the brain and thus can cause hallucinations. Hypnotics are benzos, so they enhance GABA effect (GABA = calm). Hydromorphone isn’t a benzo. b. Asking Ms. Umbridge about various aspects of her pain, such as onset, palliation factors, describing the quality of the pain, and its quantification. Always try to assess FIRST. c. Understanding the Margo McCaffery maxim that pain should always be carefully described and documented exactly as seen by the healthcare provider. Nope—pain is what the patient says it is, not what the observer “sees.” d. Knowing that with any SSRI antidepressant like this one, one has to be aware of the black box warning against increased suicidal tendencies. Very true that many antidepressants have a blackbox warning about increased suicidal tendencies but remember to pay attention to the stem of the question—it is asking about a med that is NOT an SSRI. (The reason that so many antidepressants can increase risk of suicide is that when a person is suicidally depressed, they often don’t actually have the energy to think of a plan and go through with it. Sometimes, after being on an antidepressant for a little while, their thought processes clear up and energy comes back, and then before the actual depression can lift them out of suicidal thoughts, they go ahead and commit the act.) 8. Ms Umbridge is in the hospital for several days receiving regular doses of hydromorphone. Which is true? a. She will need a daily laxative, because hydromorphone activates opioid receptors in the bowel, causing “calming” of peristalsis and subsequent constipation. b. Constipation is likely because opioids have anticholinergic side effects, which include slowing of parasympathetic stimulation of the GI tract. c. If the patient is switched to an oral pain reliever such as oxycodone, a fairly large dose will initially be needed, since oxycodone is considerably weaker than hydromorphone. d. All the above. 9. You notice that a patient begins having some muscle stiffness, slight tongue-rolling motions and drooling, and mild lip smacking. a. You believe she is having a side effect of too much benzodiazepine and may progress to having respiratory problems. Benzodiazepines don’t cause this problem. b. You are concerned that too much dopamine suppression has occurred from the phenothiazine medication she is taking, and the patient is now having EPS symptoms. A question and answer like this needs step-by-step critical thinking. Students often get confused about the link between oversuppression of dopamine (a risk when a person is on a phenothiazine drug like Thorazine)and S&S of EPS (that is, the same kind of S&S that people with Parkinson’s have). 1. First, what does dopamine do? (See ADDENDUM) It fine-tunes motor movement. Also it modulates elements of behavior and cognition, motivation and reward, mood, attention, and learning. 2. Secondly, what we know about the mechanism of psychoses, and especially schizophrenia (a type of psychosis), is that it is thought to be partly a problem of too much dopamine or overactive dopamine in certain areas of the brain, causing those elements mentioned above to be skewed, resulting in a reality- breach. Delusions, hallucinations, and socially unacceptable behaviors can result. 3. Drugs like chlorpromazine—Thorazine-- (in the phenothiazine class) suppress that overactivity, so that in essence things become “real” again. 4. The problem is, if you suppress dopamine too much, the person starts having disorders of movement (remember, dopamine is important in motor fine-tuning) such as tremors and also the ability to control fine-movements like facial expressions. The result can be either strange repetitive movements of the face (like in the video I directed you to) or someone who resembles a Parkinson’s patient—having no movement at all in their face—a very flat affect; and very jerky movements of the body These are known as extrapyramidal, or EPS, S&S. See pic in this site: 5. So the tongue rolling and lip-smacking is part of this picture of EPS S&S, caused by not enough dopamine from the over-effect (too much) of chlorpromazine (Thorazine). c. Your biggest priority is to halt the progression of tardive dyskinesia, brought on by too much dopamine being released by the patient’s anti-psychotic medications. If not noticed and no intervention takes place, the tongue-rolling and lip-smacking can become an irreversible syndrome called tardive dyskinesia. But this answer is wrong because tardive dyskinesia is brought on by suppression of dopamine, not “too much” dopamine. d. It is likely that the patient is not receiving enough chlorpromazine and must have her dosage increased. The opposite is true—the dosage should be decreased if these S&S are seen. 10. A patient describes her pain as “a burning, shooting pain traveling down my legs” that she has had for several months. Which is most likely? a. This is neuropathic pain, and may need many pain-relieving modalities such as an opioid plus adjuvant meds such as gabapentin (Neurontin) and an antidepressant. b. This is nociceptive pain and can be specifically blocked at the site of induction by a medication such as ketorolac (Toradol). ketorolac is an antiinflammatory that works at the induction site but the wrong part of this answer is that the patient is describing neuropathic pain, not nociceptive pain. c. It sounds like the patient has acute neuropathic pain that would respond well to an analgesic such as pancuronium (Pavulon). Does pancuronium help with pain? No, it only paralyzes, and you’d only give it to someone who is on a ventilator because it will paralyze the diaphragm as well as the other muscles of the body. d. It sounds like the patient has chronic back pain causing sciatica that would respond well to a dose of propofol (Diprivan). Propofol is a general anesthetic and will cause unconsciousness, which is sort of drastic for pain relief, right? Major overkill! And is it EVER given in a home setting without supervision, etc? No, never—only in a setting with monitors and people to closely watch respiratory status, etc. 11. What is true about fluoxetine (Prozac) and amitriptyline (Elavil)? a. Each is an example of different drug classes, but both block the transmission of serotonin across a synapse to receptors. No, they block reuptake of serotonin, so that there is actually more serotonin available to reach the receptors on the other side of a synapse. (“Reuptake” = a normal process of removing extra molecules of a substance to be recycled or metabolized. Decreasing/blocking reuptake = more molecules are left in the synapse to be used; in this case, serotonin, which is a neurotransmitter that basically enhances “good” feelings, etc). b. They both decrease levels of epinephrine and serotonin at nerve endings. In a different way, this is saying the essentially the same thing as answer A. c. They work in different ways, but both increase the level of serotonin in the synapse between neurons and receptor sites. fluoxetine is an SSRI—selectively blocks serotonin reuptake, and amitriptyline blocks reuptake of serotonin and others; point is that when reuptake is blocked, more of the substance is available. d. Both decrease MAO (monoamine oxidase) and thus inhibit excitatory impulses that cause the S&S of schizophrenia. A nonsense answer—mixes up MAO inhibition with (used for depression) with schizophrenia. e. A and D. 12. Your patient is receiving a drug that suppresses certain activities in the arachidonic pathway. All the following could be true EXCEPT: a. The patient is on a systemic steroid that suppresses only phospholipase and therefore has minimal side effects. Phospholipase is an enzyme which is part of the very beginning of the arachidonic pathway and enhances the development of everything thereafter, including the development of both pro-inflammatory and protective versions of prostaglandins (PGs). Steroids block that enzyme, thus having great anti- inflammatory effect (blocking pro-inflammatory PGs); but they also block the protective PCs, and that’s why there are many side effects. b. An NSAID such as ibuprofen may cause gastric ulcers because of suppression of COX 1 and COX 2. c. A COX 2 inhibitor will suppress inflammatory S&S without causing suppression of protective prostaglandins. Remember that COX2 is the subset enzyme that specifically enhances development of the pro-inflammatory aspect of prostaglandins, and not the protective aspect. So when COX2 is specifically suppressed, ONLY the pro- inflammatory aspects are suppressed. This is a good thing! However, only one COX2 inhibitor is on the market—which is it? d. Protective-prostaglandin suppression by long-term steroid use can cause high blood pressure by decreasing flexibility of arterial vasomotor response. 13. Which is true? a. Mu receptor activation of euphoria is partially responsible for addiction to mixed agonist/antagonist drugs such as butorphanol (Stadol). Agonist/antagonist drugs do not stimulate mu receptors (See RRD2, page 10). The main reason this is important is that people addicted to opioids because of the euphoria can be given a pain med that won’t stimulate that receptor—ie, have pain relief without stimulating the addictive aspect. b. If a nurse notes that a patient has a respiratory rate of 6/minute after receiving IV fentanyl, appropriate action may include opioid receptor-blocker, naloxone (Narcan). For this you needed to know normal RR and think first, “Is a RR of 6/min adequate for oxygenation?” Answer is of course “no” (norm = 12 to 20). Next: “What might have caused a RR of 6? Aha! Side effect of opioids—respiratory depression. I need to give the antidote!” c. Respiratory and cough depression are examples of problems associated with kappa receptor activation by an opiate. Kappa receptors are not associated with respiratory issues. d. While heavily sedated from large doses of oxycodone, a patient can have significant mu receptor activation, have suppression of his gag reflex, and aspirate vomitus into his lungs. Same principles as in answer B. e. A good drug that will comfort a patient in opiate withdrawal is naloxone (Narcan). A person who is opiate-dependent will have a great deal of discomfort if you give him an opioid blocker like naloxone. f. B and D. g. A and C. 14. A patient is being switched from an MAOI to citalopram (Celexa—an SSRI). Which statement made by the patient reflects understanding of patient education? a. “I can just stop taking my selegeline and start taking the Celexa right away.” Seligiline is an MAOinhibitor, and the body needs more time to re-build the enzyme monoamine oxidase (MAO) before taking another drug that needs that enzyme for metabolization. So usually healthcare providers warn patients to wait for a 2-3 weeks after stopping MAOIs before taking other psychotherapeutic meds. b. “The doctor told me to call right away if I start having muscle spasms, sweating, or shivering after I’ve been on Celexa for a while.” These are S&S of serotonin syndrome. If a person gets too high a dose of an SSRI or any other drug that increases serotonin levels, they may get too much stimulation from the serotonin and should be warned to watch for those S&S. c. “I will need to limit my intake of cheese when taking Celexa to prevent a rise in my blood pressure.” Cheese and other substances are prohibited in the case of possible interactions with MAOIs. But Celexa is an SSRI, so this prohibition doesn’t apply. (For the test, you may be asked about certain drugs, but if they are not mentioned on the drug template, I will ask about them in a certain fashion, such as, “a patient is taking Lexapro, which is an SSRI…”) d. “The doctor is switching me to this medication because it is less expensive.” There are certain situations where a less expensive drug will be just as good as the more expensive one, so a good prescriber will indeed keep cost in mind for the patient. But the stem of this question doesn’t hint at economical issues, so this answer choice would not be a good match. 15. While assessing a patient on a ventilator in the ICU a nursing student notices that the patient opens his eyes and has a frightened expression. The student mentions this to her RN preceptor, who correctly directs the student, a. “The ability of the patient to open his eyes shows that we need to give another dose of Pavulon in order to meet the objective of complete muscle paralysis while on the ventilator” b. “We need to increase the rate of the propofol drip because the current amount is not working in keeping the muscles paralyzed.” propofol is an anesthetic, not a neuromuscular blocking drug (NMBD). c. “Don’t worry about giving any more pain medicine; the NMBD, called pancuronium, is keeping the patient free of pain.” NMBDs do not give pain relief. d. “We need to increase the propofol dose in order to keep the patient sedated and unaware of the frightening effect of complete muscle paralysis.” e. A and D. The NMBD is used to prohibit the patient’s muscles from “fighting” the ventilator (it is very unpleasant to be on a ventilator—the body naturally “fights”) and propofol is used so that the patient won’t be aware of that “unpleasantness” and also of any pain he might be having. 16. Important educational information to give a patient includes a. “Avoid the usual diarrheal side-effects of oxycodone by cutting back on fiber and other foods that stimulate peristalsis.” All opioids like oxycodone tend to cause constipation, not diarrhea. b. “Since nausea is a very rare side effect anyway, it is best to take prednisone on an empty stomach.” Nausea is very common with oral steroids. c. “Herbs such as feverfew should be avoided when on NSAIDs because of additive anti- coagulant effect.” To understand this answer, remember that NSAIDs such as ibuprofen work by blocking COX enzymes in the arachidonic pathway. In turn, the end-product of the pathway—prostaglandins—are suppressed. It’s great that their pro-inflammatory aspects are suppressed, because the person then has less inflammation and thus less pain. BUT the protective prostaglandin effects are suppressed, too, including their role in enhancing clotting. Feverfew has similar effect, both good and bad, as NSAIDs. d. “Thankfully there are very few adverse effects of OTC analgesic medications, so for your frequent headaches, you can take Tylenol as much as you want.” 17. A patient’s family brings him into the ER because he has not been taking his medication(s) and they are worried about the S&S he is having. You as the patient’s ER nurse assess him. Which statement is correct about your conclusions? a. The patient is pacing, talking non-stop, and telling you about his latest shopping trip; he has likely not been taking his lithium. Typical S&S of mania. Lithium is given for the disorder known as manic-depression. b. When asked his name, the patient answers “James Tiberius Kirk,” captain of the USS Enterprise;” the patient has likely not been taking his amitriptyline. This answer showed a delusion, thus the patient is more likely has schizophrenia than depression, which is what amitriptyline is for. (Unless he really IS James T. Kirk!  ) c. The patient has a flat affect and answers questions in monosyllables; he has likely not been taking his pentazocine. The patient has typical depression S&S. Pentazocine is a pain reliever, not an antidepressant. d. The patient states he is overwhelmed by free-floating anxiety; he has likely not been taking his tramadol. Tramadol is a type of pain reliever. An anxiolytic drug like a benzodiazepine would be more appropriate. Pearl: Remember that all parts of an answer must be correct, as well as each part having sensical linkage to the other part. 18. For the patient in question 9, you will report your assessment findings and conclusions, and ask the prescriber if you should a. give Romazicon, since it is the reversal agent for this situation. b. increase the dosage of the patient’s Thorazine in order to increase dopamine and thus decrease EPS effects. c. give benztropine, which will decrease EPS symptoms by suppressing acetylcholine and allowing dopamine effects to get back to normal in the brain. See the rationale for #9. We established that the patient was having EPS S&S. Benztropine is an anticholinergic, so what it does is suppress ACh. When ACh is suppressed, dopaminergic effects are “allowed” to become stronger. This is difficult to understand unless you understand the nature of the relationship of dopamine & ACh in the brain. See the ADDENDUM. d. discontinue the anti-psychotic medication, because it is probably the re-uptake of serotonin that is causing the EPS effect. 19. During a hospital stay for a severe exacerbation of asthma, a patient receives methylprednisolone (Solu-medrol) 250mg IVPush BID. After 3 days, he comments to the nurse, “You know, I’ve noticed that my arthritis seems better these last few days. I’m not having nearly as much pain as I usually do. Is that my imagination?” The nurse explains why this is not the patient’s imagination, basing the explanation on the knowledge that a. steroids like the one the patient is receiving modulate the “perception” part of the pain pathway, so the patient perceives that his chronic pain is better. b. the steroid is calming the pro-inflammatory prostaglandins that cause both the swollen bronchi of asthma and the swollen, painful joints. c. NSAIDs like methylprednisolone suppress the enzyme cyclooxygenase, thus suppressing the creation of pro-inflammatory prostaglandins that are often the cause of pain in the body. Methylprednisolone is a steroid, not an NSAID. The rest of the answer is correct— both NSAIDs and steroids suppress creation of pro-inflammatory prostaglandins (though they do it at different points in the arachidonic pathway.) d. steroidal suppression of phospholipase stimulates the protective prostaglandin effect of providing pain relief. 20. You work as an NP in a university health clinic. A student comes to the health clinic complaining of restlessness, agitation, diaphoresis, and tremors. Which action or thinking process is correct? a. You diagnose serotonin syndrome. b. These might be S&S of opiate withdrawal. c. The student might be having a panic attack, which is an extreme manifestation of anxiety. d. You will not be able to come to a diagnosis without further assessment information, since any of the above answers could be a match for the patient presentation. 21. The patient in the question above is likely a. having withdrawal from the opiate agonist Talwin, and the S&S are caused by opioid receptor overload. Some of the S&S above could be from opiate withdrawal, but they would stem from lack of opioid receptor stimulation (not overload). b. taking fluoxetine (Prozac), and the S&S are caused by too much availability of the excitatory neurotransmitter, serotonin. c. in need of reassurance and a parenteral dose of ketorolac to calm his anxiety. Ketorolac is an anti-inflammatory, not an anxiolytic. d. having psychotic S&S and should be started on an anticholinergic drug such as benztropine. Benztropine and other anticholinergics which would suppress ACH would be appropriate for EPS S&S as noted in another question, but they have the potential of making the psychosis itself worse by increasing dopaminergic effects indirectly. 22. A patient admitted to the hospital with a diagnosis of pneumonia asks the nurse why she is receiving codeine when she does not have any pain. The nurse’s response is based on knowledge that codeine also can be used as a. a cough suppressant because of CNS (central nervous system) depression of the cough reflex . b. an anti-inflammatory that will selectively suppress COX-2 enzymes and thus limit bronchial swelling. Note: this answer is wrong, but it is a good example of how you can use these assignment questions and answers to widen your studying… for instance you could ask yourself, “1) Do I know what COX-2 is? 2) Do I know what a COX-2 inhibitor would do? 3) How does a COX-2 inhibitor differ from a non-selective NSAID? c. an anti-anxiety agent that enhances dopaminergic receptors, causing restfulness. d. a cough suppressant because codeine has cholinergic actions that dry the lung secretions. Opiates such as codeine do have a drying effect on secretions, but that effect is anticholinergic. Be sure you really understand the difference between cholinergic and anticholinergic. We studied those terms (and anticholinesterase) in Test 1 material and they are concepts that you must “bring with you” through the rest of the semester material (and always in your nursing practice). 23. Which is true? a. Ingestion of tyramine increases suppression of neurotransmitters in the body and enhances effect of MAOIs. An MAOI drug suppresses the action of MAO (monoamine oxidase). MAO is a natural enzyme in neural synapses which breaks down neurotransmitters such as norepinephrine, to be recycled etc (similar to cholinesterase for ACh). So inhibition of this process increases availability of certain neurotransmitters (NOT suppression) and this can “stimulate” the brain out of its depression. Ingestion of tyramine (found in certain foods) is like ingesting MORE of the very substances that the MAOIs have increased—so a type of additive effect. This includes an increase in norephinephrine, which increases BP and can cause hypertensive crisis. Nowadays this tyramine effect is not considered as crisis-causing as it used to be, but you should still warn your MAOI patient against overdoing certain dietary substances. b. Selegiline (Eldepryl) transdermal patch prevents MAO from breaking down dopamine and other neurotransmitters, thereby lifting depressive mood. c. Tardive dyskinesia is an EPS side-effect brought on by sub-effective dose of phenothiazines such as chlorpromazine (Thorazine). No, EPS effects are brought on by over-effect of phenothiazines in suppressing dopamine. d. All the above. First, in the box below, match up items on the right to items on the left. Each item on the left ONLY has one best answer. Do not use answers more than once. Then, for 24-30 below, choose the correct answers. • In which case might you see the following prescriber order: “Give regular insulin 2units subcutaneously if finger-stick blood glucose level is greater than 120.” (blood glucose normal = 70-99). 4_ 1. Meperedine. • A patient becomes orthostatic. 6_ 2. A very potent opiate for patients with chronic pain who have been on some type of opiate for a while. • Urate crystals causing pain. 8_ 3. Monoamine oxidase is needed to break down tyramine, so an MAOI would inhibit that; more tyramine possible hypertensive crisis. • fentanyl (Duragesic) patch 2_ 4. Patient taking prednisone, because of its chemical structure. • Works by suppressing dopamine, which for schizophrenics is thought to be in “overdrive,” causing break from reality and hallucinations. 10_ 5. Morphine (MS) • Nursing implications include having patient avoid tyramine-containing food. 3_ 6. BP goes from 120/80 when lying down to 80/40 when standing, due to opiate relaxation of arteries. • Avoid giving, especially to elderly, because of its potentially toxic metabolites. 1_ 7. Best route for opiate-naïve patients, because effects are gradual. • Watch for high serum AST & ALT. 11_ 8. Prescriber would give allopurinol, since it suppresses body’s manufacture of uric acid. • Works by inhibiting reuptake of both norepinephrine and serotonin. 12_ 9. Fluoxetine. • Can cause urinary retention & miosis because of anticholinergic side-effects. 5_ 10. Chlorpromazine. 11. Acetaminophen toxicity. 12. Tricyclic antidepressant (TCA) 24. A patient becomes orthostatic. a. 4 b. 5 c. 6 Anything that causes increased arterial vessel relaxation will cause a lowering of blood pressure. simple physics: any fluid-filled elastic-type vessel that has less tone to it (ie, is “relaxed”) will have less pressure inside it than a very toned, firm vessel. Opiates, benzos, and various other drugs have this characteristic—they relax arteries (and other blood vessels) and thus can lower blood pressure, and if the patient sits up suddenly, they may feel faint because there is not enough pressure to push blood and O2 to the brain. Sometimes we say, “the patient is orthostatic” because their BP drops and they feel dizzy when they go from lying down to sitting up. Nursing implications: tell your patient to change positions slowly, step by step—from lying down to slowly sitting up, waiting a couple of minutes, then slowly standing up. d. 11 25. Works by inhibiting reuptake of both norepinephrine and serotonin. a. 12 b. 9 c. 10 d. 8 26. In which case might you see the following prescriber order: “Give regular insulin 2units subcutaneously if finger-stick blood glucose level is greater than 120.” (blood glucose normal = 70-99). . a. 8 b. 1 c. 4 Remember that steroids’ full name is “glucocorticoids,” so they are sugar-based substances and can thus increase blood sugar. But also, you may remember from patho, that cortisol (the main steroid in the body) is a counterregulatory hormone—that is, it stimulates glycogenolysis—breakdown of glycogen—and also gluconeogenesis, when you need extra glucose in your blood. So, artificial steroids do the same thing—their side effect is to cause release of glucose into the blood hyperglycemia. If someone needs to be on steroids for a long time, we have to think about giving them insulin to bring their blood glucose down to normal levels. (see pg 9 of template) d. 11 27. Works by suppressing dopamine, which for schizophrenics is thought to be in “overdrive,” causing break from reality and hallucinations. a. 1 b. 10 c. 9 d. 12 28. Watch for high serum AST & ALT. a. 5 b. 6 c. 11 d. 2 29. Urate crystals causing pain. a. 8 Gout is a disease in which you cannot easily breakdown uric acid in a normal way & then get rid of it as needed. Instead, uric acid (AKA urate) builds up and can crystallize in the joints, causing a great deal of pain. Allopurinol is a drug that works at the “front end” of all of that and diminishes the creation of uric acid in the body in the first place. b. 12 c. 9 d. 4 30. fentanyl (Duragesic) patch a. 7 fentanyl patches are very strong and NOT for those who have never been on opioids before; other opioids are titrated and then if this patch is still needed, the patient can be on it without as much a fear of respiratory depression. b. 8 c. 2 see above. d. 1 31. When exemplary nursing student Jem Finch puts together a nursing care plan to treat the nursing diagnosis of “pain” on his patient, he will include use of a multi-modal therapy approach such as a. giving the patient no more than 2mg of the ordered “2-4 mg IVpush q 3-4 hours” morphine (MS) dose because insomnia is a frequent adverse effect of too much morphine. A side effect of MS is more likely to be excess sleepiness, not insomnia. b. suggesting the patient try acupuncture for his chronic pain, if ok with his prescriber. c. giving steroids to target the opioid receptors of the spinal cord. d. encouraging the patient to take deep, diaphragmatic breaths in order to postpone asking for pain medications for as long as possible. Slow deep breathing is usually a good non- medical approach to almost anything. However, as far as pain goes, the patient with pain should usually be told to ask for pain meds before the pain increases to a level that would make it more difficult for the meds to do their job. 32. Which is true about propofol? a. It has a limited distribution in the body because of its lipophilic properties, and therefore is used only for conscious sedation, not general anesthesia. b. Its lipophilic properties make it ideal to cross the blood-brain barrier and render a patient unconscious very quickly. c. Nursing implications for propofol include monitoring the patient for at least 48 hours after discontinuation, because of its long half-life. It has a very short half-life (a short time before the drug is on its way to being eliminated from the body), making it ideal for using during procedures because the patient only needs to be assessed for a short time before we can send them home without fear of respiratory depression. d. In educating about oral propofol use at home, the nurse should tell the patient that he should not drive because he might feel sleepy. 33. Patients taking lithium a. only need occasional blood levels drawn, since it has a wide therapeutic range. Lithium has a narrow therapeutic range. “Narrow therapeutic range” usually means a drug is unpredictable; thus in most instances blood levels will be drawn on a pretty regular basis to make sure the levels are in therapeutic range; if not, the dosage may need adjusting. Refresh your memory about this subject if you need to, in RRD 1. b. tend to be very compliant about staying on their meds, since being manic is unpleasant. c. need education about keeping their salt intake at a stable level, since lithium works by altering Na+ transport in certain nerve cells. d. should not use lithium batteries in their households, as it will cause an additive effect.  34. Patients taking antipsychotic medications a. are sometimes not compliant because the “positive” schizophrenic S&S that include hyper-energy and delusions are more desired than being stabilized to a neutral mood. True: remember that one cause of schizophrenia (which is a psychosis) is thought to be too much dopamine. This sometimes causes voices, delusions, and unpredictable thoughts & behavior, which can be scary to the patient, but in a way can also be stimulating and interesting. Medications can often get rid of these S&S, leaving a patient feeling “flat.” b. need to be educated about serotonin syndrome, since anti-psychotic meds work by inhibiting its re-uptake. No, they work by suppressing dopamine. c. should be instructed take herbal supplements that have a high dopamine and low ACh content so that neurotransmitters in the brain will be balanced. d. should be warned that the antihistamine side effects of this class of meds may cause excess salivation and lacrimation. Antihistamines have anticholinergic effects of dry mouth. (Remember I said that you have to still remember about cholinergic vs anticholinergic stuff that you learned in Test 1 material.  ) 35. You are in the ER triaging several overdose patients and realize that the one with the highest risk of death is because . a. the 17-year-old who accidentally took 9 extra-strength Tylenols over a three-day period: his liver will immediately fail and cause immediate death. Liver problems following acetaminophen overdose don’t usually occur this quickly and don’t always cause death. What med might be ordered to diminish the chance of liver failure? b. a 22-year-old who overdosed on her mother’s amitriptyline pills : TCAs have no antidote and have a dangerous cardiac dysrhythmia effect.. c. the elderly man with cancer who got confused and used too many Duragesic patches : there is no antidote for fentanyl. Wrong—there is a reversal drug…what med would you use for him? d. a child who ate his dad’s alprazolam pills thinking they were candy : the antidote for opiates cannot be used on children. 36. A person who is talking rapidly about several different subjects, using extravagant gestures, and pacing the floor a. may need to have blood tests that include a lithium level. b. is in a manic phase of bipolar disease. c. probably has a blood alcohol level of 0.10. d. may have high levels of cocaine metabolites in his urine test. e. is exhibiting classic signs of heroin use. f. A, B, and/or D. g. B, C, and/or E. 37. An RN about to give educational information to a patient who has been started on the SSRI, Celexa, looks up the drug in his reference book. What would he include in his teaching to the patient and family? a. To be watchful for any thoughts or behaviors that suggest suicidal ideation, since there is a black box warning about this. b. Description of S&S of allergic reaction, since there is a black box warning about increased susceptibility. c. If the patient is on any other SSRI, he should discontinue it immediately. No…first of all, almost NO psychotropic drug should be discontinued quickly. (For that matter, many other categories of drugs should be weaned down, rather than abruptly stopped, too—remember steroids?) Secondly, quite a number of people are on two or more SSRIs that each work in a slightly different manner and have an additive effect. d. To be aware that since depression is a type of psychosis, the patient could have increased numbers of hallucinations. Depression is not a psychosis, but rather an affective disorder. Be sure to read the basic S&S of the various mental disorders that are in your text (the descriptions are not in-depth, and that’s ok—you just need to know the differences between the various disorders so that you understand why particular drugs are being given.) 38. You are assessing someone with a severe, chronic, autoimmune disease. Which is true? a. The patient is likely on zidovudine (AZT), since this drug helps to decrease numbers of the causative virus in the blood. Think through this answer: What is AZT for? HIV infection. Is that an autoimmune disease? No, it is the opposite—an immunodeficient disease. b. An immunoglobulin shot of MMR will likely be needed as a booster to the immune system. MMR is not an immunoglobulin shot. It is a vaccination. Be sure you know the difference. c. There will likely be S&S of chronic suppression of protective prostaglandins, since the patient will likely be on long-term steroids for this disease. Read the stem of this question and this answer closely and think critically: What kind of problem is an autoimmune disease? One in which the body attacks itself and causes inflammation. What do you give for inflammation? Steroids, because they suppress the proinflammatory prostaglandins. But they also suppress the protective effect of prostaglandins, thus putting the patient at risk for a variety of side-effects related to this. d. Since the patient is likely on chloroquine, you will need to assess for malaria-related anemia. 39. In which case is pain being properly addressed? a. The teenager with osteosarcoma who is wearing a fentanyl patch and also received a large dose of hydromorphone IV push is now laughing with his friends. b. The patient who strained his back now feels better because the ketorolac he received is suppressing pain-causing prostaglandins. c. A person with nociceptive pain who receives a drug that blocks release of substance P. d. All the above. 40. Which is a correct statement? a. A person with a joint infection should be given an immunosuppressant such as prednisone to help diminish swelling and increase healing. b. After an organ transplant, a patient should be on the antibiotic cyclosporine as an empirical preventive measure against infection. He should be on cyclosporine, but it is not an antibiotic—it is an immunosuppressant. c. A prescriber discontinuing a patient’s long-term steroids should wean the doses down in a gradual fashion to allow the body to “re-boot” its own steroid manufacturing. When a person has been on steroids for a while, it suppresses the body’s natural glucocorticoid manufacturing, so if the synthetic steroid is suddenly discontinued, a person would suddenly be without any steroidal influence. An example: Cortisol is one of the hormones that helps stimulate glycogenolysis as a stop-gap measure when you are hypoglycemic between meals. Suddenly without it, you could become symptomatically and maybe dangerously hypoglycemic. d. Cushing’s syndrome is a rare drug-drug interaction event that is the result of taking herbs such as St. John’s wort while on long-term steroids. Cushing’s syndrome can be considered a conglomeration of side effects related to the suppression of the protective prostaglandins. Has nothing to do with St. John’s wort.