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NR565 Midterm Pharm Study Notes, Exams of Nursing

Atlantic Institute of Oriental Medicine (ATOM)Nursing

NR565 Midterm Pharm Study Notes

Typology: Exams

2025/2026

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NR565 Midterm
Pharm Study Notes
Week 1
•- Drug Schedules Descriptions of each schedule
•Examples of drugs in each schedule
Schedule I Controlled Substances
Substances in this schedule have no currently accepted medical use in the United
States, a lack of accepted safety for use under medical supervision, and a high
potential for abuse.
Some examples of substances listed in Schedule I are: heroin, lysergic
acid diethylamide (LSD), marijuana (cannabis), peyote, methaqualone,
and 3,4-methylenedioxymethamphetamine ("Ecstasy").
Schedule II/IIN Controlled Substances (2/2N)
Substances in this schedule have a high potential for abuse which may lead to
severe psychological or physical dependence.
Examples of Schedule II narcotics include: hydromorphone (Dilaudid®),
methadone (Dolophine®), meperidine (Demerol®), oxycodone (OxyContin®,
Percocet®), and fentanyl (Sublimaze®, Duragesic®). Other Schedule II narcotics
include: morphine, opium, codeine, and hydrocodone.
Examples of Schedule IIN stimulants include: amphetamine (Dexedrine®,
Adderall®), methamphetamine (Desoxyn®), and methylphenidate (Ritalin®).
Other Schedule II substances include: amobarbital, glutethimide, and
pentobarbital.
Schedule III/IIIN Controlled Substances (3/3N)
Substances in this schedule have a potential for abuse less than substances in
Schedules I or II and abuse may lead to moderate or low physical dependence or
high psychological dependence.
Examples of Schedule III narcotics include: products containing not more than 90
milligrams of codeine per dosage unit (Tylenol with Codeine®), and
buprenorphine (Suboxone®).
Examples of Schedule IIIN non-narcotics include: benzphetamine (Didrex®),
phendimetrazine, ketamine, and anabolic steroids such as Depo®-Testosterone.
Schedule IV Controlled Substances
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NR565 Midterm

Pharm Study Notes

Week 1

    • Drug Schedules Descriptions of each schedule
  • Examples of drugs in each schedule Schedule I Controlled Substances Substances in this schedule have no currently accepted medical use in the United States, a lack of accepted safety for use under medical supervision, and a high potential for abuse. Some examples of substances listed in Schedule I are: heroin, lysergic acid diethylamide (LSD), marijuana (cannabis), peyote, methaqualone, and 3,4-methylenedioxymethamphetamine ("Ecstasy"). Schedule II/IIN Controlled Substances (2/2N) Substances in this schedule have a high potential for abuse which may lead to severe psychological or physical dependence. Examples of Schedule II narcotics include: hydromorphone (Dilaudid®), methadone (Dolophine®), meperidine (Demerol®), oxycodone (OxyContin®, Percocet®), and fentanyl (Sublimaze®, Duragesic®). Other Schedule II narcotics include: morphine, opium, codeine, and hydrocodone. Examples of Schedule IIN stimulants include: amphetamine (Dexedrine®, Adderall®), methamphetamine (Desoxyn®), and methylphenidate (Ritalin®). Other Schedule II substances include: amobarbital, glutethimide, and pentobarbital. Schedule III/IIIN Controlled Substances (3/3N) Substances in this schedule have a potential for abuse less than substances in Schedules I or II and abuse may lead to moderate or low physical dependence or high psychological dependence. Examples of Schedule III narcotics include: products containing not more than 90 milligrams of codeine per dosage unit (Tylenol with Codeine®), and buprenorphine (Suboxone®). Examples of Schedule IIIN non-narcotics include: benzphetamine (Didrex®), phendimetrazine, ketamine, and anabolic steroids such as Depo®-Testosterone. Schedule IV Controlled Substances

Substances in this schedule have a low potential for abuse relative to substances in Schedule III. Examples of Schedule IV substances include: alprazolam (Xanax®), carisoprodol (Soma®), clonazepam (Klonopin®), clorazepate (Tranxene®), diazepam (Valium®), lorazepam (Ativan®), midazolam (Versed®), temazepam (Restoril®), and triazolam (Halcion®). Schedule V Controlled Substances Substances in this schedule have a low potential for abuse relative to substances listed in Schedule IV and consist primarily of preparations containing limited quantities of certain narcotics. Examples of Schedule V substances include: cough preparations containing not more than 200 milligrams of codeine per 100 milliliters or per 100 grams (Robitussin AC®, Phenergan with Codeine®), and ezogabine.

  • Which ones can and can not be prescribed by nurse practitioners ➢ They can prescribe all but schedule 1 because they are not legal. Varies by state
  • Prescriptive Authority
  • Understand what prescriptive authority is and who mandates it. ➢ State mandates it under the jurisdiction of the health professional board. (state board of nursing, board of medicine or board of pharmacy). Federal government controls drug regulations but has no control over prescriptive authority. Prescriptive authority is the legal right to prescribe drugs. Full authority is being able to prescribe independently without limitations. MDs and DOs have no limits. Limitations are tied to oversight of the doctor or DO. Being able to prescribe independently means is not subject to rules requiring physician supervision or collaboration. Florida III-V collaborative.
  • What problems arise when it is limited? ➢ Barriers include quality, affordable, and accessible patient care. Can increase patient waits
  • Know the responsibilities of prescribing ➢ Must consider cost, availability, interactions with either food or other medications, side effects, allergies, how the drug is metabolized (hepatic or renal), need for monitoring (labs, effectiveness, ect) special populations (pregnancy, nursing mothers, or older adults)
  • Know patient reasons for medication non-adherence ➢ Missed a dose, forgot to take a dose, did not refill medication in time, took lower than prescribed dose, did not refill medication, stopped taking medication. ➢ Reason why includes forgot a dose, ran out, was away from home, trying to save money, did not like the side effects, was too busy, the medication didn’t work, didn’t believe medication was necessary, didn’t like taking the medication. Failure to comprehend instructions for reasons such as visual, intellectual or auditory impairment, use of complex regimens (taking several drugs multiple times a day)

may not achieve therapeutic levels. They are Carbamazepine, rifampin, alcohol, phenytoin, griseofulvin, phenobarbital, sulfonylureas. Pneumonic is CRAP GPS induces my rage to memorize. Inhibitors act on the liver through a process known as inhibition. By slowing the rate of metabolism, inhibition can cause an increase in active drug accumulation. This can lead to an increase in adverse effects and toxicity. They are Valproate, Ketoconazole, Isoniazid, Sulfonamides, Chloramphenicol, Amiodarone, Erythromycin, Quinidine, Grapefruit juice. https://youtu.be/OhIopfQm9_w Video helps the breakdown of how it works

  • Be familiar with opioid agonists ➢ Agonists are molecules that activate receptors. Because neurotransmitters, hormones, and other endogenous regulators activate the receptors to which they bind, all of these compounds are considered agonists. When drugs act as agonists, they simply bind to receptors and mimic the actions of the body's own regulatory molecules. For example, dobutamine is a drug that mimics the action of NE at receptors on the heart, thereby causing heart rate and force of contraction to increase. In terms of the modified occupancy theory, an agonist is a drug that has both affinity and high intrinsic activity. Affinity allows the agonist to bind to receptors, whereas intrinsic activity allows the bound agonist to activate or turn on receptor function. Full agonists bind tightly to the opioid receptors and undergo significant conformational change to produce maximal effect. Examples of full agonists include codeine, fentanyl, heroin, hydrocodone, methadone, morphine, and oxycodone. The pure opioid agonists activate μ receptors and κ receptors. By doing so, the pure agonists can produce analgesia, euphoria, sedation, respiratory depression, physical dependence, constipation, and other effects. The pure agonists can be subdivided into two groups: strong opioid agonists and moderate to strong opioid agonists. Morphine is the prototype of the strong agonists. Codeine is the prototype of the moderate to strong agonists.
  • Know the outcome of having a poor metabolism phenotype ➢ A poor-metabolizing enzyme has very low activity. It is possible to have side effects even with a very low drug dose, because the enzyme is very slow to break down the drug
  • Know the role of the government agencies when it comes to prescription drugs Week 2
  • Know black box warning for various pain medications. ➢ The boxed warning , also known as a black box warning , is the strongest safety warning a drug can carry and still remain on the market. Text for the warning is presented inside a box with a heavy black border. The FDA requires a boxed warning on drugs with serious or life-threatening risks. The purpose of the warning is to alert providers to (1) potentially severe side effects (e.g., life-threatening dysrhythmias, suicidality, major fetal harm) as well as (2) ways to prevent or reduce harm (e.g., avoiding a teratogenic drug during pregnancy). The boxed warning provides a concise summary of the adverse effects of concern. A boxed warning must appear prominently on the package insert, on the product label, and even in magazine advertising. Drugs that have a boxed warning must also have

a MedGuide. An example of a drug with a boxed warning is promethazine (Phenergan). Promethazine is contraindicated in patients less than 2-years-old because it can cause respiratory depression. Additionally, when administered by injection, there is a risk for severe tissue injury and necrosis. Opioid medications can cause respiratory arrest in both opioid-naïve and opioid-tolerant patients. Monitor for respiratory depression, especially during new-onset therapy or after escalation of dose. Fentanyl Products containing fentanyl can cause fatal respiratory depression. Many of these products are only available through restricted distribution programs secondary to misuse and abuse. Methadone Methadone prolongs the QT interval and hence may pose a risk for potentially fatal dysrhythmia. Torsades de pointes has developed in patients taking 65 to 400 mg/day. To reduce risk, methadone should be used with great caution—if at all—in patients with existing QT prolongation or a family history of long QT syndrome and in those taking other QT-prolonging drugs. In addition, methadone causes severe respiratory depression that can be potentially fatal. Hydromorphone and Oxymorphone Hydromorphone and oxymorphone have high abuse potential and can cause fatal respiratory depression, especially when used in combination with other sedating agents such as alcohol. Long-acting forms of oxymorphone should be prescribed only by a provider with additional education regarding chronic pain. Codeine In the liver, about 10% of each dose of codeine undergoes conversion to morphine, the active form of codeine. The enzyme responsible is CYP2D6 (the 2D6 isoenzyme of cytochrome P450). Among ultrarapid metabolizers, which carry multiple copies of the CYP2D6 gene, codeine is unusually effective and has led to death in some children. Severe toxicity can also develop in breastfed infants whose mothers are taking codeine. The cause is high levels of morphine in breast milk, due to ultrarapid codeine metabolism. Oxycodone Like oxymorphone and hydromorphone, oxycodone has a high potential for abuse and can cause fatal respiratory depression. Long-acting forms of oxycodone should be prescribed only by providers with additional education regarding chronic pain. Hydrocodone All forms of hydrocodone contain a black box warning. Products that contain acetaminophen (Vicodin) are associated with hepatotoxicity. The extended-release forms of hydrocodone can cause fatal respiratory depression and should only be prescribed by providers with additional education regarding chronic pain.

  • Be familiar with patient indicators that would put them at risk for developing substance abuse disorder.

➢ Multiple prescribers given prescription drugs, refill requested early

  • When is it appropriate to prescribe naloxone? ➢ Naloxone (Narcan) is a structural analog of morphine that acts as a competitive antagonist at opioid receptors, thereby blocking opioid actions. Naloxone can reverse most effects of the opioid agonists, including respiratory depression, coma, and analgesia. Naloxone is the drug of choice for treating overdose with a pure opioid agonist. The drug reverses respiratory depression, coma, and other signs of opioid toxicity. Naloxone can also reverse toxicity from agonist-antagonist opioids (e.g., pentazocine, nalbuphine). However, the doses required may be higher than those needed to reverse poisoning by pure agonists. ➢ Dosage must be carefully titrated when treating toxicity in opioid addicts because the degree of physical dependence in these individuals is usually high and hence an excessive dose of naloxone can transport the patient from a state of poisoning to one of acute withdrawal. Accordingly, treatment should be initiated with a series of small doses rather than one large dose. Because the half-life of naloxone is shorter than that of most opioids, repeated dosing is required until the crisis has passed. If the patient received a dose of naloxone by a friend or family member for a suspected overdose, the patient should be transported by emergency providers to the nearest emergency department for further evaluation. ➢ In some cases of accidental poisoning, there may be uncertainty as to whether unconsciousness is due to opioid overdose or to overdose with a general CNS depressant (e.g., barbiturate, alcohol, benzodiazepine). When uncertainty exists, naloxone is nonetheless indicated. If the cause of poisoning is a barbiturate or another general CNS depressant, naloxone will be of no benefit—but neither will it cause any harm. ➢ Should be prescribe if patients are at risk for opioid use disorder, have a history of nonfatal overdose, higher dose opioids (>50 MME/day), concurrent benzo use You may want to consider prescribing naloxone for the following patients at risk:
  • Be familiar with drugs that are not safe to take with opioids. ➢ Benzos, other substances, alcohol,
  • Be familiar with the PEG Assessment Scale. ➢ PEG stands for Pain average, interference with Enjoyment of life, and interference with General activity Assessment scale. Helps track patient outcomes. Clinically meaningful improvement has been defined as a 30% improvement in scores for both pain and function. Monitoring progress toward patient centered function goals, such as walking the dog or walking around the block, returning to work part time, can also contribute to the assessment of functional improvement. 0-10 scale - Patients taking benzodiazepines concurrently with opioids - Patients receiving high opioid dosages (≥ 50 MME per day) - Patients diagnosed or suspected of having OUD - Patients with a history of nonfatal overdoses - Patients who have concurrent alcohol or substance use Naloxone can cause acute withdrawal symptoms with adverse effects in patients physically dependent on opioids. Caution must be exercised with a review of needs, benefits, and risks.

➢ Question 1. what number describes your pain on average in the past week 0 (no pain)- 10 (pain as bad as you can imagine) ➢ Question 2. What number best describes how, during the past week, pain has interfered with your enjoyment to life? 0 (does not interfere) -10 (completely interferes) ➢ Question 3. What number best describes how, during the past week, pain has interfered with your general activity 0 (does not interfere) – 10 (Completely interferes)

  • Patient and provider responsibilities in opioid drug therapy ➢ Risk vs benefits, policies of practice, follow up, ➢ Patient responsibilities ➢ Provider responsibilities
  • How to approach conversations about Opioid Use Disorder ➢ Open and honest discussion, non-confrontational
  • What types of pain can be treated by psychotropic medications? ➢ Neuropathic pain, postherpetic neuralgia, fibromyalgia, migraines, diabetic neuropathy. Examples are pregabalin, gabapentin, carbamazepine, TCA’s and SNRI’s o Taking all medications as prescribed o Keeping appointments with provider o Committing to all recommended therapies o Acknowledging risks and side effects o Communicating any questions or concerns o Participating in urine drug testing (UDT) o Disclosing the use of other medications, including OTC and illicit drugs o Keeping medication in a safe place, away from other people (including children) o Communicating expected benefits and risks throughout therapy, at least every three months o Recommending a multimodal therapy approach, combining nonopioid and nonpharmacologic therapies with opioid therapy to improve effectiveness o Reviewing the PDMP and UDT o Reviewing refill requests carefully to ensure opioid medication is used appropriately
    • Heart Failure
  • o Role of aldosterone and how to manage those effects
  • HF activates the RAAS. Activation occurs in response to reduced blood pressure and reduced renal blood flow. When activated, the RAAS promotes water retention by increasing circulating levels of aldosterone and angiotensin II. Aldosterone acts directly on the kidneys to promote the retention of sodium and water. Aldosterone also has more harmful effect which include
  • • Promotion of myocardial remodeling (which impairs pumping)
  • • Promotion of myocardial fibrosis (which increases the risk for dysrhythmias)
  • • Activation of the SNS and suppression of norepinephrine uptake in the heart (both of which can promote dysrhythmias and ischemia)
  • • Promotion of vascular fibrosis (which decreases arterial compliance)
  • • Promotion of baroreceptor dysfunction
  • Management includes aldosterone antagonists— spironolactone

(Aldactone) and eplerenone (Inspra) Aldosterone

antagonists work primarily by blocking aldosterone

receptors in the heart and blood vessels. These drugs can

cause hyperkalemia. Drugs can reduce the effects of

aldosterone by either decreasing aldosterone production

or blocking aldosterone receptors. agents that inhibit the

RAAS can be highly beneficial. Four groups of drugs are

available: ACEIs, ARBs, direct renin inhibitors (DRIs), and

aldosterone antagonists. BBW for spironolactone is it is

associated with tumorigenesis in case study rats.

➢

    • Who is at risk for severe rebound hypertension? ➢ Rebound hypertension occurs when blood pressure rises after you stop taking or lower the dose of a drug (typically a medicine to lower high blood pressure ). This is common for medicines that block the sympathetic nervous system like beta blockers and clonidine. Can occur when there is an abrupt discontinuation of many different antihypertensive drugs
    • Be familiar with treatment guidelines of hypertension. ➢ See HTN sheet
  • o When one medication would be preferred over another based-on patient factors
    • Mechanism of action and related physiological outcomes
  • o Cardiac glycosides (Digoxin) known for positive inotropic actions. Increase myocardial contractile force by inhibiting the enzyme known as sodium-potassium

adenosine triphosphatase (Na+,K+-ATPase) and increase cardiac output. As a

result of increased cardiac output, three major secondary responses occur: (1) sympathetic tone declines, (2) urine production increases, and (3) renin release declines. These responses can reverse virtually all signs and symptoms of HF.

However, they do not correct the underlying problem of cardiac remodeling.

Potassium competes with digoxin so if potassium levels are low digoxin levels increase and cause toxicity and if potassium levels are high digoxin level is reduced and impaired therapeutic response. It is imperative to keep potassium levels WNL while on dig. Used in Heart failure and a fib but is not shown to prolong life in HF. Second line agent now for HF. It has a profound neurohormonal effect. Can cause severe dysrhythmias and has a small window for a therapeutic dose. May shorten life in women. Patient education should include to monitor their heart rate and signs and symptoms of dig toxicity which include altered heart rate or rhythm, visual or gastrointestinal disturbances. o Verapamil -calcium channel blocker indicated for HTN, Angina, Dysrhythmias, and migraine and work on the arterioles and the heart. Can have toxic doses that produce dangerous cardiac suppression. By blocking calcium channels in the heart and blood vessels, verapamil has five direct effects:

  • • Blockade at peripheral arterioles causes dilation and thereby reduces arterial pressure.
  • • Blockade at arteries and arterioles of the heart increases coronary perfusion.
  • • Blockade at the SA node reduces heart rate.
  • • Blockade at the AV node decreases AV nodal conduction. Most important
  • • Blockade in the myocardium decreases force of contraction
    • SE include constipation, dizziness, facial flushing, headache, edema in feet or ankles. Can increase dig toxicity and interact with grapefruit juice
    • o Organic nitrates ➢ nitroglycerin is first choice. It is a vasodilator. Decrease oxygen demand by dilating veins and decreases preload, increases oxygen supply by relaxing coronary vasospasm. Fast acting and inexpensive. Acts directly on vascular smooth muscle to promote vasodilation and converts to its active form nitric oxide but requires the sulfhydryl enzyme. Nitro does not affect coronary blood flow. Highly lipid soluble and half-life is 5- 7 minutes. Can cause orthostatic hypotension, reflex tachycardiac.
    • o Calcium channel blockers ➢ Used to treat HTN, angina, and dysrhythmias. Effects are on the blood vessels and the heart. They prevent calcium ions from entering the cell. Controversy in patients with diabetes and hypertension. Calcium entry plays a critical role in the function of vascular smooth muscle and the heart. Calcium channels regulate contraction and when channels

Rosuvastatin 20- mg Atorvastatin 10- mg Rosuvastatin 5- mg Simvastatin 20– mg Moderate-Intensity Statin Therapy Approximately^ 30%^ to^ <50% Pravastatin 40- mg Lovastatin 40 mg Fluvastatin XL 80 mg Fluvastatin 40 mg BID Pitavastatin 2– 4 mg Low-Intensity Statin Therapy Approximately <30% Simvastatin 10 mg Pravastatin 10– mg Lovastatin 20 mg

Fluvastatin 20– mg Pitavastatin 1 mg ➢

    • Alternative treatment strategies for stain intolerant patients ➢ Statins are contraindicated in pregnancy and should use Ezetimibe and fibrates should be used if benefits outweigh the risks.