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Pharmacology > Exam 1 > Flashcards

Exam 1 Flashcards

1
Q

9 rights of medication administration

A
  1. Right Drug: correct drug is given, medication orders must be checked against the medication label or profile three times before giving the medication. (During initial preparation of medication; before removing from storage place
    Is drug appropriate?
    Correctly ordered?
    Before you place the unit dose pkg in medicine cup
    Before you open the unit dose pkg at the bedside
  2. Right Dose: confirm dosage amount is appropriate for age and size, pediatric and elderly patients are more sensitive to medications than adults, thus use extra caution with drug dosage.- check 3 times
  3. Right Time: routine medication no more than .5 hour before, stat medications no later than .5 hour after, or single order given only once, or standing order written in advance under specific circumstances, or prn, as required, as needed. Use military time when recording medication in medical records
  4. Right Route & Form: oral suspension, tablet, capsule, gelcap, pediatric drops, and rectal suppository. Controlled Release drugs cannot be crushed or altered.
  5. Right Patient
  6. Right Documentation: correct documentation is the sixth right of medical administration, document date, time, name, dosage, route, pertinent lab values, VS and site. Only document after the medication has been given, do not use trailing zeros. Negative changes in symptoms experienced, AE/SE, toxicity, drug-related physical and/or psychological symptoms
    Improvement
    If drug is not administered, document why and any actions taken.
  7. Right Reason or Indication: appropriateness in use of medication, confirm the rationale
  8. Right Response: assess and evaluate the drugs response in the patient; Document assessment findings, interventions, monitoring
  9. Right to refuse: document the refusal, Make sure the client understands the medication, Inform the prescriber, Document refusal and continue to monitor
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2
Q

Understand the principles related to documentation of medication administration

A 
- Document AFTER the med has been given
Include: 
- Date & time
- Route
- Pertinent lab values
- VS
- Document drug action
- Negative changes in symptoms experienced
- AE/SE, toxicity
- drug-related physical and/or psychological symptoms
- Improvement 
- If drug is not administered, document why and any actions taken.
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3
Q

Identify incomplete/incorrect written prescriptions

A

Medication, Dose, Route, Times?

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4
Q

Differentiate between objective and subjective assessment data

A
  • Objective: what is observed

- Subjective: what the patient or family tells you

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5
Q

Identify the different components of the nursing process

A
  • Assessment
  • Diagnosis (nursing statement)
  • Plan
  • Implementation
  • Evaluation
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6
Q

Additional rights of nurses

A
  • Right to a “double check” and constant system analysis (e.g. system f drug admin. Process w/regard to everyone involved, including the doctor, nurse, nursing unit, pharmacy dept. and with regard to client education.)
  • Right to proper drug storage & documentation
  • Right to accurate calculation and preparation of dosage of med and proper use of all types of medication delivery systems.
  • Right to careful checking of the transcription of medication orders
  • Right to pt safety with correct procedures and techniques of med admin.
  • Right to accurate routes of admin. And specific implications.
  • Right to close consideration of special situations (e.g. client with difficulty swallowing, pt w/NG tube, unconscious pt)
  • Right to having all measures taken with regard to the prevention and reporting of med errors
  • Right to individualized and complete client teaching
    Right to accurate and cautious pt monitoring for therapeutic effects, side effects, & toxic effects
  • Right to continued safe use of the nursing process with accurate documentation in narrative form or in SOAP (Subjective, objective, assessment, planning) notes format
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7
Q

Who can prescribe drugs in Missouri and Kansas

A
  • Physician assistants can prescribe Schedules II-V controlled if outlined in the supervision of agreement w/physician. May not prescribe Schedule II controlled. Verbal orders have to be signed within 24 hours, or as per guidelines within hc institution.
  • Dental hygienists w/direct access: can provide services without supervision in public health settings to Medicaid-eligible children and can be directly reimbursed. Have to have 3 years of experience and may provide oral prophylaxis, sealants, and fluorides
  • Nurse practitioners: require written collaborative practice agreements w/ a physician. Agreement must outline geographic practice areas for the physician and the NP and methods of treatment within an NP’s scope of practice. NPs are not explicitly recognized in state policy as primary care providers. Prescriptive authority & privileges must outlined in the written agreement. and be within the NP’s scope of practice. Can prescribe
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8
Q

abbreviations for extended- release

A 
CR – controlled release
LA – long acting
SR – sustained release
TR – timed release
RD – time delay
SA – sustained action
XL – extended release
XR – extended release
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9
Q

Time releasing drugs

A
  • Many drugs in psychiatry have been time-release formulated to reduce their local adverse effects in the gastrointestinal tract, to reduce adverse effects associated with peak blood levels, or to artificially extend their half-life.
  • Time-release formulations are associated with the added advantages of convenience of dosing, improved compliance, and less fluctuation in blood levels across the course of the day.
  • A disadvantage of time-release formulations is that they may be incompletely absorbed; this is a serious issue in patients with acute or chronic intestinal hurry disorders, such as gastroenteritis or irritable bowel syndrome. more expensive than immediate-release formulations.
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10
Q

Identify which patients will likely have the most difficulty metabolizing drugs.

A
  • Cardiovascular dysfunction, Renal insufficiency
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11
Q

Know which type of drugs will NOT undergo first-pass effect.

A
  • Drugs administered by the intravenous route
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12
Q

Understand how drugs have their mechanisms of action

A
  • Receptor Interactions: joins the drug molecule with the reactive site on the surface of the cell or tissue, then interacts with the receptor for a pharmacologic response. The drug becomes bound to the receptor through the formation of chemical bonds between the receptor on the cell and the active site on the drug molecule.
  • Enzyme Interactions: drug chemically binds to an enzyme molecule that alters (inhibits or enhances) the enzyme’s interaction.
  • Nonselective Interactions: physically interfere with or chemically alter cellular structures or processes.
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13
Q

Review why older adult clients may have a lower dose of a drug in relation to pharmacokinetics

A
  • Their systems function slows down so with older adults you want to start drugs with a low slow dose.
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14
Q

Identify considerations for pediatric clients in relation to pharmacokinetics and drug absorption.

A
  • Pediatric patients organs are not fully developed yet, so you need to take into consideration that their function may not work the same because they have immature organs.
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15
Q

Know which clients will have the most difficulty excreting drugs

A
  • Renal dysfunction
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16
Q

Know the differences between allergic and idiosyncratic reactions

A
  • An allergic reaction is a hypersensitivity, idiosyncratic is an abnormal unexpected response to a medication peculiar to an individual
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17
Q

Pharmacokinetics

A
  • the study of what happens to a drug from the time it is put into the body until the parent drug and all metabolites have left the body. Includes the phases absorption, distribution, metabolism, excretion, drug’s onset of action, time to peak effect, and duration of action
  • Absorption: movement of a drug from site of administration into bloodstream for distribution to tissues.
  • Affected by process and route of administration.
  • Quantified by bioavailability which is the extent of drug absorption.
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18
Q

Pharmacodynamics

A

the study of biochemical and physiologic interactions of drugs; what the drug does to the body. It examines the physiochemical properties of drugs and their pharmacologic interactions with suitable body receptors. More specifically, the mechanism of action

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19
Q

Pharmacotherapeutics

A

the treatment of pathologic conditions through the use of drugs.

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20
Q

Pharmaceutics

A

Science of preparing and dispensing drugs, including dosage form design.
Formulation of different drugs determines rate of dissolution and absorption.

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21
Q

Enteral route

A
  • Drug is absorbed into systemic circulation through the mucosa of the stomach and/or small or large intestine.
  • Oral
  • Sublingual
  • Buccal
  • Rectal (can also be topical)
  • Typically this route is the slowest for absorption of drugs.
  • The sublingual route is the fastest of these because the drug is absorbed into the highly vascularized tissue under the tongue.
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22
Q

Parenteral route

A
  • Intravenous (fastest delivery into circulation)- invasive
  • Intramuscular
  • Subcutaneous
  • Intradermal
  • Intraarterial
  • Intrathecal
  • Intraarticular
  • injections such as IV, IM, and subQ.
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23
Q

Topical route

A
  • Skin (transdermal patches)
  • Eyes
  • Ears
  • Nose
  • Lungs (inhalation)
  • Rectum
  • Vagina
  • take longest for absorption to occur
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24
Q

what is the first-pass effect?

A
  • A drug that is absorbed from the intestine must first pass through the liver before it reaches the systemic circulation.
  • If a large proportion of a drug is chemically changed into inactive metabolites in the liver, than a much smaller amount of drug will pass into the circulation (i.e. be bioavailable). - Such a drug is said to have a high first pass effect.
  • First-pass effect reduces the bioavailability of the drug to less than 100%.
  • Many drugs given orally have a bioavailability of less than 100% but drugs given by the IV route are 100% bioavailable.
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25
Q

what are the only 2 routes that undergo the first pass effect

A
  • enteral

- oral

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26
Q

what are non-first pass routes

A
  • A drug that is absorbed form the intestine must first pass through the liver before it reaches the systemic circulation.
  • If a large proportion of a drug is chemically changed into inactive metabolites in the liver, than a much smaller amount of drug will pass into the circulation (i.e. be bioavailable). - Such a drug is said to have a high first pass effect.
  • First-pass effect reduces the bioavailability of the drug to less than 100%.
  • Many drugs given orally have a bioavailability of less than 100% but drugs given by the IV route are 100% bioavailable.
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27
Q

what routes are for non-first pass routes?

A
  • Sublingual: Absorbed into the highly vascularized tissue under the tongue, the oral mucosa.
  • Buccal: Absorbed into the highly vascularized tissue of the cheek.
  • Parenteral or Injection (Subcutaneous (SC), Intradermal, Intramuscular (IM),
    Intravenous (IV))
  • Topical (Transdermal, Inhalation, Intranasal, Intraocular, Vaginal)
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28
Q

What is Pharmacokinetics distribution?

A
  • transport of a drug by the bloodstream to its site of action
  • Only drug molecules that are not bound to plasma proteins can freely distribute to extravascular tissue to reach their site of action.
  • If a drug is bound to protein, the drug-protein complex is generally too LARGE to pass through the walls of blood capillaries into tissues.
  • Drugs are distributed first to those areas with extensive blood supply.
  • Areas of rapid distribution include the heart, kidneys, liver, and brain.
  • Areas of slower distribution include muscle, skin, and fat. - Once a drug enters the bloodstream it is distributed throughout the body.
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29
Q

Protein binding of drugs

A
  • Drugs can be freely distributed to extravascular tissue only when not bound to protein.
  • This unbound portion is pharmacologically ACTIVE and considered “free” drug.
  • Drugs that bind to albumin: acidic drugs, phenytoin, warfarin, digoxin, naproxen, ceftriaxone, lorazepam, valproic acid
  • A drug’s efficiency is affected by the degree to which it binds to proteins within the blood.
  • The LESS BOUND a drug is, the more efficiently it can travel cell membranes and navigate to its site of action.
  • A drug’s performance can be enhanced or decreased by protein binding.
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30
Q

Drugs that are highly protein bound

A

More acidic drugs bind to albumin:

  • phenytoin (AED)
  • warfarin (anticoagulant)
  • digoxin (antidysrhythmic, heart failure)
  • naproxen (antiinflammatory)
  • ceftriaxone (antibiotic)
  • lorazepam (benzodiazepine for anxiety)
  • valproic acid (AED, manic phase of bipolar, migraine headaches)
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31
Q

what are two sites where it is difficult to distribute drugs?

A
  • bone
  • blood-brain barrier
  • drugs must be injected straight into site of action
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32
Q

What organ is most responsible for the metabolism of most drugs?

A

The liver is the organ most responsible for the metabolism of drugs.

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33
Q

What client factors can cause variations in the metabolism of drugs?

A

Client factors include liver disease, genetic diseases, liver failure.

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34
Q

Cytochrome P-450 enzymes

A
  • also known as microsomal enzymes
  • Target lipid-soluble drugs (lipophilic: “fat loving”), which are typically difficult to eliminate
  • Most drugs are lipophilic!
    There are other drugs that are water-soluble (hydrophilic: “water loving”)
  • Easily metabolized by chemical reactions
  • patients who have a deficiency of the cytochrome P-450 enzyme system are going to have more difficulty metabolizing drugs
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35
Q

Fast and Slow acetylators

A

“slow” acetylator :
- a person who has an autosomal recessive single gene trait which effects the N-acetylate transferase enzyme in the liver.
- This gene causes the enzyme to work slowly in the metabolism of certain drugs.
Because of this slow pace situation, “slow” acetylators will receive more of the given drug in circulation than a fast acetylators who is metabolizing the drug and excreting it (via kidneys).
- show a greater therapeutic response than fast acetylators to several drugs (e.g., isoniazid, hydralazine).
- may also be more susceptible to the side effects mediated by acetylated metabolites, such as isoniazid hepatotoxicity and lupus-like syndrome after hydralazine or procainamide.

Fast acetylation:

  • autosomal dominant genetic trait.
  • may not reach therapeutic levels with treatment and require greater doses.
  • Fast: up to 50% of the population in Canada, Germany & as low as 10% among some American Indians and the majority of Eskimos and Asians
  • Slow: up to 50% of African Americans and Caucasians
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36
Q

What organ is responsible for elimination of drugs from the body?

A
  • Kidneys

- Few meds are excreted by the intestines and biliary system.

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37
Q

Half-life

A
  • Time it takes for one half of the original amount of a drug to be removed.
  • Measure of the rate at which drugs are removed from the body.
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38
Q

onset

A

time it takes for a drug to elicit a therapeutic response.

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39
Q

peak

A

time it takes for a drug to reach its maximum therapeutic response.

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40
Q

duration

A

time that drug concentration is sufficient to elicit a therapeutic response.

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41
Q

peak level

A

highest blood level

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42
Q

trough level

A

lowest blood levels

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43
Q

drug toxicity

A

peak blood is too high

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44
Q

Mechanism of action

A
  • describes how drugs work.
  • This means how the specific drug works, or what action it has in the body.
  • Drugs produce actions (therapeutic effects) by:
    1. Modifying the rate at which the targeted cell or tissue functions
    2. Modifying the function of the targeted cell or tissue
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45
Q

Receptor and Enzyme interactions

A
  • Drugs act by forming a chemical bond w/specific receptor sites, similar to a key and lock.
  • The better the “fit” the better the response.
  • Drugs with complete attachment and response are called agonists.
  • Drugs that attach but do not elicit a response are called antagonists.
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46
Q

Drug receptor interactions

A
  • Agonist: binds to the receptor > response occurs
  • Partial agonist: binds to receptor > response diminishes
  • Antagonist: binds to receptor > no response Prevents binding of agonists
  • Competitive antagonist: competes w/the agonist for binding. If binds, no response
  • Noncompetitive antagonist: combines w/different parts of receptor & inactivates it. Agonist then has no effect.
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47
Q

Reasons for giving therapeutic medications

A
  • Acute: vasopressors to maintain BP and CO after open heart surgery
  • Maintenance: does not eradicate the problem but will prevent progression of the disease or condition. Examples: BP meds. Oral contraceptives for birth control
  • Supplemental: supplies body with substance needed for normal function: example: insulin for DM
  • Palliative/supportive: example: high dose opioids for final stages of cancer
  • Prophylactic therapy: antibiotics active against the organism commonly associated with a specific infection
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48
Q

Medication effects to monitor

A
  • Contraindications/cautions: this means reasons to either not give the drug or to use it cautiously. Each drug has its own set of contraindications/cautions. (allergy contraindication for every drug)
  • Therapeutic response: this is the desired effect of the drug.
  • AE’s/SE’s: these are the non-desired effects of drugs.
    Therapeutic index:
  • Low therapeutic index: difference between therapeutically active dose & toxic dose is small. Requires close monitoring.
  • Drug concentration: this is the amount of drug in the blood
    Interactions: drugs can interact with food or other drugs and produce undesired effects or increase therapeutic effects.
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49
Q

Tolerance

A

a decreasing response to repeated drug doses. (need higher dose)

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50
Q

Dependence

A
  • Dependence: physiologic or psychological need for a drug
  • Physical dependence: physiologic need for a drug to avoid physical withdrawal symptoms
  • Psychological dependence: also known as addiction and is the obsessive desire for the euphoric effects of a drug
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51
Q

Adverse Drug Reactions

A
  • Pharmacologic:
    extension of drug’s normal effects
  • Allergic (hypersensitivity)
    Involves immune response; immune system recognizes the drug, a drug metabolite, or an ingredient in the drug as dangerous, foreign.
  • Idiosyncratic: Pharmacologic:
    extension of drug’s normal effects; Genetically inherited traits that result in the abnormal metabolism of drugs are universally distributed throughout the population.
  • Drug interactions: when 2 drugs interact & produce an unwanted effect. Can be the result of 1 drug either making the other one more potent & accentuating its effects or diminishing the effectiveness of the other. Drug interactions can be intentional & beneficial, too.
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52
Q

Additive effect

A

1 + 1 = 2

  • When two drugs with similar actions are given together.
  • GOOD THING
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53
Q

Synergistic effect

A

1 + 1 = 3

  • 2 drugs are combined & results in effects that are greater than the effect that could have been achieved if either 1 drug was given alone.
  • Drug synergy, the combined boost of drug efficacy, is a highly pursued goal of combinational drug development.
  • Synergistic drug combinations have been shown to be highly efficacious and therapeutically more specific.
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54
Q

Antagonistic effect

A

1 + 1 = 0

  • BAD THING
  • Combined drug effects are less than those that could have been achieved if either drug was separately.
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55
Q

Incompatibility

A
  • commonly refers to parenteral drugs.
  • Chemical deterioration of drug
  • Produces precipitate, haziness, or a change in color of the solution
  • Seen a lot in intravenous drugs- see if the two drugs are compatible without chemical deterioration of the drug
  • May have to start another iv if incompatible
  • check incompatibility chart
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56
Q

Adverse drug event (ADE)

A
  • An injury caused by a medication or failure to admin. An intended medication. May or may not be preventable (i.e. due to error); may or may not cause pt harm. Includes all ADRs but is not always caused by a med error (ME). Also includes expected or anticipated side effects of medications.
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57
Q

Adverse drug reaction (ADR)

A

Any unexpected, unintended, undesired, or excessive response to a medication at doses normally used for prophylaxis, diagnosis or therapy and results in hospital admission, prolongation of hospital stay, change in drug therapy, initiation of supportive trtmt, and complication of dx disease state.

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58
Q

ADR- side effects

A
  • expected, well-known rx resulting in little or no change in pt mgmt. They have predictable frequency.
  • Intensity and occurrence are r/t size of the dose.
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59
Q

ADR- serious adverse events

A

are serious adverse events. These are defined as events that are fatal, life threatening, or permanently/significantly disabling; requiring or prolonging hospitalization; cause congenital anomalies, or require intervention to prevent permanent impairment or damage.

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60
Q

Identify appropriate strategies for administering medications to a toddler.

A
  • Provide a brief concrete explanation about injections
  • Make use of magical thinking
  • Provide comfort measures after the injections
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61
Q

Review appropriate dosing guidelines for drugs given to older adults.

A
  • Medications will be of smaller doses, be aware of their medications because of an increased risk of interaction
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62
Q

the differences in risks associated with administering drugs in the first and third trimesters of pregnancy.

A
  • 1st trimester: greatest danger for drug-induced developmental defects, Drug exposure is more detrimental during the 1st trimester.
  • 3rd trimester: Drug transfer is more likely, Transfer of drugs occurs through diffusion across the placenta.
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63
Q

Identify physiologic differences that affect pharmacokinetics in neonatal and pediatric patients.

A
  • Absorption, distribution, metabolism, and excretion are for the most part decreased.
  • Absorption: Gastric pH is less acidic, first pass is reduces, intramuscular absorption is faster and irregular
  • Distribution: fat content is lower, protein binding is decreased, more drugs enter the brain because of an immature blood-brain barrier
  • Metabolism: microsomal enzymes are decreased, increased metabolism, status of liver enzyme production
  • Excretion: Glomerular filtration rate and tubular secretion and resorption are decreased, perfusion of kidneys may be decreased
    Still anatomic structures & physiologic structures still developing
  • Dosages should be severly decreased
  • Some organs are not fully developed yet so worry about potential drug toxicity
  • May have unusual drug responses due to organs not fully developed
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64
Q

Drug therapy during breastfeeding

A
  • A great number of drugs can cross from mother’s circulation into breast milk.
  • Drug levels are usually lower than in maternal circulation, but must consider risks vs. benefits
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65
Q

Calculating drug dosage in pediatric patients

A
  • Body Weight: Most commonly used method today
  • Dosages based on milligrams (mg) per kilogram (kg) of body weight
  • Need to know 1 kg = 2.2 pounds
  • Body Surface Area:
    Uses a specific formula to calculate dosage
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66
Q

Consideration for elderly with drugs

A
  • Drug therapy likely to result in AEs & toxicities due to:
    Polypharmacy, Physiologic changes, Pharmacokinetics
  • Absorption is slowed.
  • Distribution is decreased.
  • Metabolism is decreased.
  • Excretion is decreased.
  • START LOW AND GO SLOW
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67
Q

purpose of using placebo drugs in investigational drug trials.

A

Separate out the real benefits from the apparent benefits

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68
Q

the ethical principles and the nursing roles associated with each

A
  • Autonomy: self determination and the ability to act on ones own
  • Beneficence: the ethical principle of doing or actively promoting good
  • Justice: ethical principle of being fair or equal in one’s actions
  • Nonmaleficence: duty to do no harm to a patient
  • Veracity: the duty to tell the truth
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69
Q

legal principles of duty and causation.

A
  • Duty: do job

- Causation: knowing the aspects that can cause malpractice

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70
Q

who maintains responsibility to the patient in cases where nursing students make a med error.

A
  • Once the student has committed a medication error, his or her responsibility is to the patient and to being honest and accountable.
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71
Q

cultural considerations for drugs

A
  • Influence of ethnicity on genetics & drug response
  • Drug polymorphism: refers to affects related to patients age, gender, size, body composition, and other characteristics on pharmacokinetics of specific drugs
  • Adherence with therapy
  • Environmental and economic considerations
  • Pharmacokinetics: also known that levels of citochrome p450 enzymes can affect different ethnic groups
  • Pharmacodynamics
  • Varying drug responses in different racial or ethnic groups
  • Health beliefs and practices
  • Barriers to adequate health care for the culturally diverse U.S. patient population
    (Language, poverty, access, pride, & beliefs regarding medical practices;
    Medications may have a different meaning to different cultures)
  • Be aware of your own beliefs and biases about racial, ethnic or cultural groups.
  • This can influence how medication is prescribed and therefore, how effective it is for a patient.
72
Q

varying drug response by racial and ethnic groups examples

A

AFRICAN AMERICANS
- respond better to diuretics than they do beta blockers and ace inhibitors
-tend to respond best to calcium channel blockers (ex. deltiazin)
-respond less to single drug therapies (multiple antihypertensive drugs prescribed)
ASIANS & HISPANICS
-might need lower doses of haloperidol or haildol
-respond better to lower doses of antidepressants because they metabolize these drugs more slowly
-Asians- metabolize antipsychotic drugs more slowly
-Japanese- metabolize antimanic drugs more slowly (need a lower dose)

73
Q

Cultural assessment

A
  • Languages spoken: need for interpreter
  • Health beliefs and practices
  • Past uses of medicine
  • Herbal treatments, folk remedies, home remedies
  • OTC drugs and treatment
  • Usual response to illness
  • Responsiveness to medical treatment
  • Religious practices and beliefs
  • Support from the patient’s cultural community
  • Dietary habits
74
Q

clinical phases of FDA drug approval process

A
  • Phase 1: small number of very healthy subjects- helps determine optimal dose range and if further testing is needed
  • Phase 2: small number of individuals with the disease- helps to see if drug is effective
  • Phase 3: large number followed by medical research centers- gives us more info about infrequent or rare adverse affects that have not been seen yet
  • Phase 4: post marketing studies- gives further proof of therapeutic affects and adverse affects of drug
75
Q

Black box warning

A
  • done if pattern of severe reactions to a newly marketed drug
  • Class I
  • Class II
  • Class III
76
Q

U.S. FDA drug approval process

A
  • Informed consent
  • Preclinical investigational drug studies
  • Clinical phases
  • black box warning
77
Q

Legal nursing considerations and drug therapy

A
  • State and federal legislation dictate boundaries
  • Nurse practice acts
  • Guidelines from professional nursing groups
  • American Nurses Association (ANA)
  • Institutional policies and procedures; state and federal hospital licensing
  • Specific Nurse Practice Acts
  • Standards of Practice
  • HIPPA
78
Q

autonomy

A

have the ability to act on own and nurse can promote patients own autonomy by having patient make their own decisions, supporting patients decisions, and supporting patients right to informed concent

79
Q

beneficence

A

doing or promoting good, nurse can help promote this by determining how patient is best served

80
Q

confidentiality

A

our duty to respect priveledge info about patient. Do not talk about with anybody

81
Q

justice

A

being fair and equal in ones own actions- ensure justice by ensuring fairness in distributing resources to patients

82
Q

nonmaleficence

A

duty to do no harm- avoid deliberate harm when caring for patient

83
Q

veracity

A

duty to tell the truth- nurse should tell the truth about placebo drug therapy, investigational new drugs, or during informed consent process

84
Q

describe the concept of just culture

A
  • Recognize systems are generally at fault, so after review, discipline is done
  • places blame on possible system errors instead of personal blame
85
Q

process of medication reconciliation.

A
  • Medications are reconciled at all points of entry and exit to/from a health care entity
  • Patients provide a list of all medications they are currently taking (including herbal products & over the counter), the prescriber then assess if they continue
  • 3 steps:
  • Verification- collection of patients drug information, focus on meds currently being used (OTC, prescriptions, herbals, supplements)
  • Clarification- medication reconciliation is professionally reviewed (review meds that were in verification phase and making sure all meds and dosages were appropriate for the patient)
  • Reconciliation- further investigation of any descrepancies or changes in medication orders
86
Q

ways to prevent medication errors

A
  • Systems of checks and balances
  • Prescribers write legible orders or electronically
  • Resources are consulted if there is any area of lack of clarity
  • Nurses check medication order three times before giving drug and consult
  • Basic nine rights of medication administration
87
Q

what are considered authoritative sources for looking up drug information.

A

Within the last five years

88
Q

examples of medication errors.

A
  • Wrong drug calculation
  • Look/Sound alike drugs
  • Poor penmanship
89
Q

adverse drug event definition

A

Undesirable occurrence r/t admin. or failure to admin a med.

90
Q

adverse drug reaction definition

A

Unexpected, unintended, excessive response to a med admin. at therapeutic dose

91
Q

allergic reaction definition

A

Immunologic reaction from sensitivity of patient

92
Q

idiosyncratic reaction definition

A

Abnormal/unexpected response; peculiar

93
Q

medication errors definition

A 
Preventable adverse drug event by patient, or hc professional (may or may not cause harm)
- steps errors can occur: (ANY!)
Procuring
Prescribing
Transcribing
Dispensing
Administering
Monitoring
Organizational issues
Educational system issues
Sociologic factors
Use of abbreviations
94
Q

Reporting medication errors

A
  • Report to prescriber and nursing management.
  • Document error per policy and procedure.
  • Factual documentation only
    (Medication administered,
    Actual dose, Observed changes in patient condition,
    Prescriber notified and follow-up orders)
  • External reporting of errors
    (United States Pharmacopeia, Medication Errors Reporting Program, MedWatch- sponsored by the Food and Drug Administration (FDA),
    Institute for Safe Medication Practices, The Joint Commission)
95
Q

Consequences for the nurse

A
  • Emotional
  • Legal – malpractice
  • Consider your own insurance!
  • Job: continued education, disciplinary action to suspension or termination
  • State Board of Nursing may require counseling, suspend or revoke license
96
Q

Nonadherance

A

Aka noncompliance, but do not call it this as it has a negative connotation to it
Nonadherence- maybe there is something else going on that is preventing the patient in taking their medication as prescribed or at all
Possible reasons: patient cannot afford medication, the medication has a problematic adverse affect that they don’t like, their culture has something to do with it, health literacy is lacking and they don’t understand how to take their medication

97
Q

difference between supplements and legend drugs

A
  • Legend drugs: not legally available without a prescription from a prescriber
  • Supplements: require no proof of efficacy and set no standards for quality control
98
Q

priority assessment for the client taking ginkgo biloba

A
  • Gingko: may increase risk for bleeding with anticoagulants and antiplatelets
99
Q

advantages/disadvantages of OTC use

A
  • Advantages:
  • conveniently and effectively self treat minor ailments
  • allows prescribers to spend more time with more serious health problems
  • Less expensive
  • Decreased overall healthcare cost
  • Disadvantages:
  • patients may not see provider until they are very ill
  • insurance companies usually won’t pay for OTC
  • Patient education is very important but we lose out on educating- always go over all meds when they come in
  • Increase out of pocket expense
  • May postpone treatment or seeking medical symptoms- eliminate symptom but not cause
  • Insurance does not cover cost
  • interactions with current prescription medications
    toxicity
  • abuse
100
Q

difference in OTC and prescription drugs

A

Prescription drugs:

  • Prescribed by a hc provider
  • Bought at a pharmacy
  • Prescribed for & intended to be used by one person
  • Regulated by FDA

OTC drugs:

  • Do NOT require a hc provider’s prescription
  • Bought off-the-shelf in stores
  • Regulated by FDA through OTC Drug monographs.
101
Q

Criteria for OTC status

A

Indication for use- consumer must be able to easily:

  • diagnose condition
  • monitor effectivenes

safety profile- drugs must have:

  • favorable adverse event profile
  • limited interaction with other drugs
  • low potential for abuse
  • high therapeutic index

practicality for OTC use- drugs must be:

  • easy to use
  • easy to monitor
102
Q

Herbal and dietary supplements

A
  • Dietary supplement—orally administered alternative medicines, including herbal supplements
  • Herbs—plant components, including bark, berries, roots, leaves, gums, seeds, stems, and flowers, used for their medicinal qualities
  • Herbal medicine—using herbs to heal
    • Plant component:
      bark, berries, roots, stems and flowers, gums, seeds
  • augment diet
  • amino acids
  • Vitamins and minerals
  • Enzymes
  • Liquids, powder, capsule, tablets, food and drink
  • About 30% of medicines are derived from plants (cocaine, popatron, atrophine, capsaysin, dejoxin, zopolamine,
103
Q

National Center for Complementary and Alternative Medicine (NCCAM)

A
  • complementary aka integrative medicine: simultaneous use of both traditional and alternative medicine.
- NCCAM classifies complementary and alternative medicine
Alternative medical systems:
- Mind–body interventions
- Biologically based therapies
- Manipulative and body-- based methods
- Energy therapies
104
Q

Consumer use of herbs

A
  • Therapeutic agents for treatment and cure of diseases
    Prophylactic agents for long-term prevention of disease
  • Proactive agents to maintain health and wellness and “boost” one’s immune system
    -adverse affects considered minimal by consumers and manufacturers
    -idea is: if it comes from the earth it must be safe
    -not regulated by the FDA
    -in 1994 BSHEA passed and defined dietary supplements and provided a regulatory framework
    -in 2002 the US pharmacopeia began certifying products that had been independently tested against its dietary supplement verification program
  • DSHEA requires no proof of ethicacy and provides no standards for quality control for supplements
    -since 2007 manufacturers must provide some sort of product identity, composition, quality, purity, and strength of the active ingredients
    -have to also demonstrate products are free of contaminants: microbes, pesticides, heavy metals
    -not necessarily safe
    -can see allergic reactions, toxic reactions, and adverse affects
    -some interact with OTC drugs
    -about 40% of clients don’t disclose to their prescriber that they use a dietary supplement
105
Q

Conditions treated with herbal products

A
  • Anxiety
  • Colds and cough (Echinacea)
  • Depression (st. johns wart)
  • Headache (fever few)
  • Insomnia (melatonin)
  • Ulcers
  • Premenstrual syndrome
  • Arthritis
  • Constipation
  • Fever
  • Infection
  • Stress
  • Weakness
106
Q

Most commonly used herbal products

A
  • Aloe
  • Feverfew
  • Gingko
  • Goldenseal
  • St. John’s wort
  • Valerian
  • Echinacea
  • Garlic
  • Ginseng
  • Hawthorn
  • Saw palmetto
  • Turmeric
107
Q

Nursing Implications for OTC, herbal, supplements, etc.

A
  • Obtain thorough medication history, documenting all medications used (prescription, OTC, herbal products, vitamins, minerals, other dietary supplements).
  • Assess level of education and understanding.
  • Assess for information specific to various products.
  • Assess system functions (especially renal, liver, and cardiac).
  • Assess for conditions that are contraindications.
  • Assess for potential drug–drug and drug–herb interactions.
  • Provide thorough and individualized client education.
  • Ensure that clients recognize that manufacturers of herbal products and dietary supplements are not required to prove safety and effectiveness.
  • Herbal products may not be safe for pregnant or breastfeeding women, infants, or children.
  • “Natural” does not mean safe.
  • Teach clients to monitor themselves for unusual or adverse reactions as well as therapeutic responses.
108
Q

ethical issues related to the Human Genome Project and gene therapy

A
  • Eugenics: intentional selectin before birth of genotypes

- Prospect of being able to manipulate genes in human germ cells

109
Q

the difference between indirect and direct gene therapy

A
  • Indirect: uses DNA vectors to help make drugs

- Direct: directly replacing one gene with another

110
Q

role of the RN as it relates to gene therapy

A
  • Knowledge of principles and application
111
Q

s/s of toxicity and overdose of Adernergics

A
  • Seizures
  • Hypo-&Hyper- Tension
  • Dysrhythmias
  • Palpitations
  • Dizziness
  • Nervousness
  • Fatigue
112
Q

AE’s for dobutamine

A
  • Mild tremor, HA, flux of bp, nervous, dizzy, Increased HR, Palpations
113
Q

Therapeutic effects of dopamine

A
  • Dilate blood vessels to the heart, brain, kidneys, mesenteries
  • Improve cardiac contractibility & output
  • Vasoconstriction
114
Q

Indications for epinephrine

A
  • Ophthalmic (vasoconstriction in the eye)
115
Q

Human Genome Project

A
  • Started in 1990; completed in 2003
  • Identified the estimated 30,000 genes and 3 billion base pairs in the DNA of an entire human genome
    Improved prevention, treatment, and cures for disease
  • Developed new tools for genetic data analysis and storage
  • Goal is to transfer exogenous genes that will either provide a temporary substitute for or initiate permanent changes in the patients own genetic functioning to treat a given disease
  • Initially this was only to be used with inherited diseases, but now there is research with gene therapy related to cancer, cardiovascular disease, diabetes, infectious diseases, substance abuse, etc.
  • They are still looking at it for the use in utero for preventing the development of serious diseases
116
Q

limitations for gene therapy

A
  • Viruses used for gene transfer can induce viral disease and can be immunogenic in the human host.
  • Proteins produced by artificial methods can be immunogenic
117
Q

In vitro manipulation

A
  • Get rid of dysfunctional gene
  • Introduce viral vector and therapeutic gene
  • Therapeutic gene self duplicates and now we have overcome that dysfunctional
118
Q

rDNA technology

A
  • Use of rDNA vectors in the laboratory to make recombinant forms of drugs:
  • Hormones, vaccines, antitoxins, and monoclonal antibodies
  • Escherichia coli bacterial genome: used to manufacture a recombinant form of human insulin
  • Most insulin today is made this way
119
Q

Regulatory and Ethical Issues Regarding Gene Therapy

A
  • National Institutes of Health (NIH) Guidelines for Research Involving Recombinant DNA Molecules:
  • Eugenics: intentional selection before birth of genotypes that are considered more desirable than others
  • U.S. gene therapy research is limited to somatic cells only
  • Gene therapy in germ-line (reproductive) cells is currently not approved for funding by the NIH
  • Use therapy to help target treatment for patient- how is genetic makeup going to change their medications, alter course of disease process
  • Make sure there is informed consent
  • Genes can only be somatic cells (not allowed to clone people)
120
Q

Pharmacogenetics

A

general term for the study of genetic variations in drug response and focuses on single-gene variations

121
Q

Pharmacogenomics

A
  • combination of 2 scientific disciplines: pharmacology and genomics
  • Involves how genetics (genome) affect the body’s response to drugs
  • Individualized therapy based on patient’s genetic makeup
  • Goal is to predict patient drug response and proactively tailor drug selections and dosages in order to have optimal outcome
  • Differ between poor and rapid metabolism with drugs
    Rapid- some people have genetic predisposition to rapidly metabolize drugs (would need higher doses of that drug)
  • Poor- don’t have the genetic predisposition and metabolize drugs more slowly
  • If we can identify the rapid metabolizers then we will have a better outcome as we will know how to specifically tailor their dosage for certain kinds of medications (warfarin, cumadin, blood thinner)
122
Q

Patient teaching for beta blockers

A
  • Take medications as prescribed
  • Never stop abruptly
  • Report constipation, u. retention, bladder distension
  • Change position slowly Os. HypoT
  • Avoid caffeine and alcohol
  • Palpations, SOB, nausea, vomiting (notify prescriber)
123
Q

Interactions for tamsulosin (Flomax)

A
  • Relax smooth muscle in prostate, bladder

- Exclusively indicated for male clients

124
Q

Indications for beta blockers (i.e. carvedilol)

A
  • Angina: myocardial demand for oxygen
  • Cardioprotective: inhibits stimulation from circulating catecholamines
  • Dysrhythmias: Class II antidysrhythmic
  • HTN
  • Heart Failure
125
Q

AE’s of cholinergic drugs

A
  • CV: bradycardia, hypotension, syncope, conduction abnormalities
  • CNS: headache, dizziness, convulsions, ataxia
  • GI: abdominal cramps, increased secretions,
  • Respiratory: increased bronchial secretions, bronchospasms
  • Other: lacrimation, sweating, salivation, miosis
126
Q

Therapeutic onset of cholinergic drugs

A
  • Stimulate intestines, contraction of pupils, increased salivation & sweating, CV effects, pulmonary effects
127
Q

Contraindications for the use of cholinergic drugs

A
  • Drug allergy
128
Q

S/S of toxicity of cholinergic drugs

A
  • Salivation, lacrimation, urinary incontinence, diarrhea, GI cramps, emesis
129
Q

Indications for cholinergic-blocking drugs

A
  • Primarily for CV disorders
130
Q

S/S of overdose of cholinergic-blocking drugs

A
  • Hyperthermia, mydriasis (pupil dilation) , flushed face, decreased secretion, thirsty
131
Q

Functions of the ANS

A
  • controls internal body processes such as the following:
  • Blood pressure
  • Heart and breathing rates
  • Body temperature
  • Digestion
  • Metabolism (thus affecting body weight)
  • The balance of water and electrolytes (such as sodium and calcium)
  • The production of body fluids (saliva, sweat, and tears)
  • Urination
  • Defecation
  • Sexual response
  • Sometimes the two divisions have opposite affect on the same organ
    Example: sympathetic will increase BP while parasympathetic will decrease BP
  • Overall the two divisions work together to make sure the body responds appropriately to different situations
  • Drugs that stimulate the sympathetic NS are known as Adrenergic agonist
132
Q

Characteristics of Adrenergic Drugs

A
  • Mimic the effects of SNS neurotransmitters (catecholamines)
    1. Norepinephrine (NE)
    2. Epinephrine (EPI): direct-acting
    3. Dopamine
  • Produce a sympathomimetic response
133
Q

Catecholamines

A
  • Drugs used therapeutically to produce the same result as endogenous catecholamines

PROTOTYPES:

  • Synthetic: Dobutamine
  • Endogenous: Dopamine (body already has it)
134
Q

Direct-Acting Sympathomimetics

A
  • bind directly to receptor & causes a physiologic response
  • PROTOTYPE: Epinephrine
135
Q

Adrenergic Drug Effects on smooth muscles

A
  • Vasoconstriction of blood vessels
  • Relaxation of GI smooth muscles (decreased motility)
  • Constriction of bladder sphincter
  • Contraction of uterus
  • Male ejaculation
  • Contraction of pupillary muscles of the eye (dilated pupils)
136
Q

Adrenergic Drug Effects on CV system

A
  • Stimulate beta1-adrenergic receptors:
  • stimulation of myocardium, AV node, & SA node
    + inotropic effect:
    ↑ force of contraction
    + chronotropic effect:
    ↑ heart rate
    + dromotropic effect:
    ↑ conduction through AV node
137
Q

Adrenergic Drug Effects on airways

A
  • Stimulation of beta2-adrenergic receptors:
  • Bronchodilation (relaxation of the bronchi)
  • Other effects of beta2-adrenergic stimulation:
  • Uterine relaxation
  • Glycogenolysis in the liver
138
Q

Adrenergic Drug Indications

A
  • Respiratory (Bronchodilators)
  • Topical Nasal Decongestant- cause constriction of dilated arterials and reduction in nasal blood flow which helps decrease congestion
  • Ophthalmic (Epinephrine)- directly to surface of the eye, like nasal decongestants but work with they eye vasculature
  • Overactive Bladder- help to relax the detrusor muscle in the bladder which leads to an increase in bladder storage capacity
  • Cardiovascular (Cardiac failure or shock)
139
Q

Adrenergic drug contraindications

A
  • drug allergy

- severe hypertension

140
Q

Adrenergic drugs adverse effects

A
  • Unwanted CNS effects-headache, restlessness, excitement, insomnia, euphoria (think about overstimulation!)-cardiovascular effects, chest pain, vasoconstriction, high blood pressure, palpations, dysrhythmias,
  • Other significant effects: Sweating, nausea, vomiting, muscle cramps
  • Toxicity:
    Extension of common adverse effects
    Seizures
    Hypotension or hypertension
    Dysrhythmias, palpitations
    Dizziness, nervousness
    Fatigue
141
Q

Adrenergic drugs interactions

A

Adrenergic agonists and adrenergic antagonists: Reduced therapeutic response for both classes of drug
Adrenergic drugs with anesthetic agents: Increase the risk for cardiac dysrhythmias
Adrenergic drugs with MAOI’s: Risk for life-threatening hypertensive crisis
Antihistamines: Increase the effects of adrenergic drugs
Thyroid preparations: Increase the effects of adrenergic drugs

142
Q

Dobutamine Beta1-selective

A
  • Structurally similar to naturally occurring catecholamine, dopamine
  • Stimulates beta1 receptors on myocardium:
    + inotropic effect: so ↑ CO & SV
  • for pts with heart failure
  • Do not give to patient with coronary artery disease or someone who has had an MI
    -adverse affect- it can actually worsen heart failure
143
Q

Dopamine Naturally Occurring Catecholamine

A
  • Potent dopaminergic, beta1- & alpha1-adrenergic receptor activity
  • Low dosages: dilates bld. vessels&raquo_space;> increases bld. flow to brain, heart, kidneys, & mesentery
  • Higher infusion rates: improves cardiac contractility & output (beta1-adrenergic receptor activity)
  • Highest doses: vasoconstriction (alpha1-adrenergic receptor activity)
  • Can cause hypertension and tachycardia
  • Interacts with MAOIs hematellin (anti-seizure drug)
  • Only given in IV infusion
144
Q

Epinephrineendogenous vasoactive catecholamine

A
  • Acts directly on both alpha- & beta-adrenergic receptors of tissues innervated by the SNS
  • Prototypical nonselective adrenergic agonist
  • Administered in emergencies, ACLS
  • Also for anaphylactic shock
  • Response to this is dose related:
  • Low doses- stimulates beta1 receptors, increase contraction of the heart, increases heart rate, can be used to treat asthma and anaphylactic shock
  • High doses- stimulates alpha adrenergic receptors which can cause vasoconstriction to elevate blood pressure
  • Made in 2 different strengths for IV use: 1-1000 or 1-10000
  • 1-1000: comes in 1mg/1mL vial
  • 1-10000: comes in .1mg/1mL vial
145
Q

Nursing Implications for Adrenergic Drugs

A
  • Assess for allergies, asthma, & history of HTN, dysrhythmias, other CV disease.
  • Assess renal, hepatic, & cardiac function
  • Assess:
    Baseline VS (postural BP & HR); temperature
    Peripheral pulses
    Skin color
    Capillary refill
  • Follow administration guidelines carefully
  • IV administration:
    Check IV site often for infiltration, extravasation
    Use only if solution is clear
    Administer on an infusion pump
    Infuse slowly to avoid dangerous CV effects
    Continuously monitor cardiac rhythm
  • With chronic lung disease:
    Instruct to avoid factors that may exacerbate condition
    Encourage fluid intake (up to 3000 mL/day), if permitted.
    Teach about proper dosing, use of equipment (MDI, spacer, nebulizer), & equipment care.
  • Administering 2 adrenergic drugs together may precipitate severe CV effects such as tachycardia or hypertension.
  • Monitor for therapeutic effects (CV uses):
    Decreased edema
    Increased urinary output
    Return to normal VS
    Improved skin color & temperature
    Increased LOC
  • Monitor for therapeutic effects (asthma):
    Return to normal breathing, RR
    Less dyspnea, breathlessness
    Improved breath sounds, fewer crackles
    Increased air exchange
    Decreased cough
    Improved blood gases
    Increased activity tolerance
146
Q

Prototypes of Adrenergic-blocking drugs

A 
- Alpha blockers: 
Tamsulosin (Flomax)
- Beta blockers:
metoprolol (Lopressor)
- Alpha & Beta blockers:
labetalol (Normodyne)
carvedilol (Coreg)
147
Q

Alpha Adrenergic Blockers: MOA

A
  • Bind to adrenergic receptors & inhibit or block stimulation of the SNS
  • Opposite effect of adrenergic drugs
  • Cause vasodilation, reduced BP, miosis, and reduced smooth muscle tone in bladder and prostate
  • Classified by type of adrenergic receptor they block:
    Alpha1 & alpha2 receptors
    Beta1 & beta2 receptors
  • Alpha blocker work either by direct competition with Epi or by a noncompetitive process
  • Alpha blockers have a greater affinity for the alpha adrenergic receptor than norepinephrine does, so this can displace norepinephrine molecules from that receptor
148
Q

Alpha adrenergic blockers: indications

A 
- Variety of uses including: 
Hypertension
Benign prostatic hyperplasia (BPH)
Pheochromocytoma
Raynaud’s disease
Frostbite
Prevent skin necrosis and sloughing following extravasation
149
Q

Alpha adrenergic blockers: contraindications

A
  • Known drug allergy
  • Peripheral vascular disease
  • Hepatic and renal disease
  • Coronary artery disease
  • Peptic ulcer
  • Sepsis
150
Q

Alpha adrenergic blockers: adverse effects

A
  • Primary AE’s are related to their effects on the vasculature:
  • “First-dose phenomenon”- severe and sudden drop in BP after administration of the first dose
  • Orthostatic hypotension
  • Dizziness, HA, constipation
  • Toxicity:
    Support of symptoms
    Focus on monitoring BP!
151
Q

prototype: Tamsulosin (Flomax)

A
  • MOA/Indication: Alpha blocker to treat BPH
    Relax smooth muscle in prostate, bladder
    Exclusively indicated for male clients
  • Contraindications: known drug allergy; concurrent use of erectile dysfunction drugs
    AE: headache, abnormal ejaculation, rhinitis
    Interactions: warfarin, antihypertensives, erectile dysfunction drugs, alcohol
  • Alpha adrenergic blocker- going to compete for alpha adrenergic receptors preventing and stimulating new spots
  • Provides relaxing effect on targeted system or organs (smooth muscle in prostate)- makes for better flow of urine
  • Used in treatment of benign prostatic hypertrophy
  • Do not give to patient with an allergy or if taking erectile dysfunction drugs
  • Warfarin- competes for same binding sites (both drugs will have decreased effectiveness)
  • Other interactions have additive effects to the drugs- have to watch for hypotension
152
Q

Beta Blockers: MOA

A
  • Block stimulation of beta receptors in SNS
  • Compete with norepinephrine & epinephrine
  • Can be selective or nonselective
  • Cardioselective beta blockers or beta1-blocking drugs
    Nonselective beta blockers block both beta1 & beta2 receptors
153
Q

Beta Receptors

A

Beta1 receptors

  • Located primarily on the heart
  • Beta blockers selective for these receptors are called cardioselective beta blockers

Beta2 receptors
- Located primarily on smooth muscle of bronchioles & blood vessels

154
Q

Beta blocker action

A 
- Cardioselective beta 1 blockers: 
Decrease HR
Slows conduction thru AV node
Prolongs SA node recovery
Decrease myocardial oxygen demand
Decrease myocardial contractility
- Nonselective beta blockers: 
CV effects of beta 1 blockers
- Block beta 2 receptors on smooth muscle of bronchioles and blood vessels: 
Smooth muscle contraction
Narrowing of airways 
Vasoconstriction 
Inhibit glycogenolysis slowing recovery from hypoglycemia
155
Q

Indications for beta blockers

A

CV:
- Angina: Decreases myocardial demand for O2
- Cardioprotective (post-MI): Inhibits stimulation from circulating catecholamines
- Dysrhythmias: Class II antidysrhythmic
- HTN
- Heart failure
CNS: Migraine headache
- Lipophilicity allows entry into CNS
- Eyes: glaucoma (topical use)

156
Q

AE/SE: Beta Blockers

A
  • Heme- Agranulocytosis, thrombocytopenia
  • CV- AV block, bradycardia, heart failure
  • CNS-Dizziness, depression, unusual dreams, drowsiness
  • GI- N/V, constipation, diarrhea
  • Other- Impotence, alopecia, wheezing, bronchospasm, dry mouth
  • Nonselective beta blockers may interfere with the body’s normal responses to hypoglycemia (i.e., tremor, tachycardia, nervousness).
  • May mask S/S of hypoglycemia
  • Use cautiously in diabetics
157
Q

LOLS prototypes

A
  • metoprolol
  • Labetalol
  • Carvedilol
158
Q

PROTOTYPE: METOPROLOL (Lopressor)Cardioselective

A
  • Most commonly used beta1-blocker
  • Indications: post-MI, HTN, stable heart failure
  • Has shown to increase survival in pts post-MI
  • Contraindications: allergy, heart block, heart failure, DM
  • AE: hypotension, bradycardia, dizziness, HF
  • Interactions: cardiac glycosides, MAOIs, cimetidine, hydralazine
  • Nursing Considerations: Taper doses when discontinuing. Check apical HR, BG & BP.
  • Looking for a decrease in HR and decrease in speed of conduction through the SA node
  • Can mask hypoglycemia
159
Q

prototype: labetalol (Normodyne

A
  • Alpha1-blocker & beta-blocker
  • Indications: severe HTN, hypertensive emergencies, quickly lowers BP
  • Contraindications: allergy, uncompensated HF, cardiogenic shock, pregnancy, bradycardia
  • AE’s: similar to metoprolol
  • Interactions: see Table 19.5
160
Q

prototype: Carvedilol (Coreg)

A
  • Nonselective beta blocker
    Indications: heart failure, HTN, angina
  • Contraindications: uncompensated HF, asthma, cardiogenic shock, advanced heart blocks
  • AE’s: dizziness, HA, hypotension, bradycardia, edema, UTI, urinary retention
  • Interactions: amiodarone, MAOI’s, cimetidine have additive effects > cause hypotension
  • Blocks beta 1 and beta 2 blockers
  • Do not give to patients with uncompensated HF
161
Q

Adrenergic-Blocking Drugs: Nursing Implications

A
  • Alpha blockers may precipitate hypotension
  • Some beta blockers may precipitate bradycardia, hypotension, heart block, heart failure, bronchoconstriction
  • Avoid OTC meds, possible interactions.
  • Drug interactions may occur with:
    Antacids (aluminum hydroxide)
    Antimuscarinics & anticholinergics
    Diuretics, CV drugs
    Neuromuscular blockers
    Oral antihyperglycemics
  • Teach:
    Take medications as prescribed.
    Should never stop abruptly.
    Report constipation or development of urinary hesitancy or bladder distention.
    Change positions slowly to prevent or minimize postural hypotension.
    Avoid caffeine (excessive irritability).
    Avoid alcohol ingestion & hazardous activities until blood levels become stable.
    Notify prescriber if palpitations, dyspnea, N/V occur.
  • Monitor for adverse effects.
  • Monitor for therapeutic effects:
    Decreased chest pain in clients with angina
    Return to normal BP and HR
    Other specific effects, depending on the use
  • Rebound HTN or chest pain may occur if discontinued abruptly.
  • Teach: Notify prescriber if they become ill and unable to take medication.
  • Teach: Assessment of BP and pulse BEFORE taking.
    Teach: May notice a decrease in tolerance for exercise (dizziness & fainting may occur with increased activity) - Notify prescriber if these problems occur.
  • Teach pts to report the following:
    Weight gain of more than 2 pounds in 1 day or 5 pounds in 1 week.
    Edema of the feet or ankles
    Shortness of breath
    Excessive fatigue or weakness
    Syncope or dizziness
162
Q

Cholinergic Drugs

A
  • Drugs that stimulate the parasympathetic nervous system (PSNS)- PSNS is the opposing system to the SNS
  • Also known as cholinergic agonists or parasympathomimetics
  • Mimic effects of the PSNS neurotransmitter acetylcholine (ACh)
  • Direct- or Indirect-acting
  • Direct- bind directly to cholinergic receptors and activate them
  • Indirect- stimulate the close synaptic release of acetylcholine at the receptor site (this allows Ach to bind and stimulate the receptor - inhibit the acetylcholinerase (enzyme responsible for breaking down Ach)
163
Q

Cholinergic Drugs: MOA

A
  • Effects of direct- and indirect-acting cholinergic drugs are seen when PNS is stimulated
  • Think ‘rest and digest’
  • Used primarily for target effects on GI system, bladder, and eye
164
Q

Cholinergics: Drug Effects

A
  • Stimulate intestines and bladder- Increased gastric secretions, GI motility, and urinary frequency
  • Stimulate constriction of pupils- Decreases intraocular pressure
  • Increase salivation and sweating
  • CV effects- Reduced HR and vasodilation
  • Pulmonary effects- Bronchi constriction and airway narrowing
165
Q

Prototype: donepezil (Aricept)

A
  • MOA:
    Indirect-acting
    Works centrally in brain to increase acetylcholine levels
  • Indications:
    Mild to moderate Alzheimer’s disease
  • Contraindications:
    Drug allergy
  • AE’s:
    GI upset, drowsiness, dizziness, insomnia, muscle cramps
    CV effects
  • Interactions:
    Anticholinergics, NSAIDs
  • inhibits acetylcholinerase
  • Mild AE that resolve on their own, can be avoided with carefully titrating the dose
  • Gi AE can increase risk for gastric uler and GI bleeding
  • CV effects- syncope, bradycardia, hypotension that reflects tachycardia, sometimes hypertension
  • Anticholinergics- would interact effects
  • NSAIDs- reduce effectiveness
166
Q

AE/SE: overstimulation of PNS

A
  • CV:
    Bradycardia, hypotension, syncope, conduction abnormalities (AV block and cardiac arrest)
  • CNS:
    Headache, dizziness, convulsions, ataxia
  • GI:
    Abdominal cramps, ↑ secretions, N/V
  • Respiratory
    Increased bronchial secretions, bronchospasms
  • Other
    Lacrimation, sweating, salivation, miosis
167
Q

Cholinergic Crisis

A
  • Circulatory collapse, hypotension, bloody diarrhea, shock, & cardiac arrest.
  • SLUDGE:
    S: Salivation
    L: Lacrimation
    U: Urinary incontinence
    D: Diarrhea
    G: GI cramps
    E: Emesis
  • Early signs:
    Abdominal cramps, salivation, flushing of the skin, nausea, and vomiting, transient syncope, transient
168
Q

Cholinergic Crisis: Treatment

A
  • In early phase: atropine, a cholinergic antagonist
  • Severe CV reactions or bronchoconstriction:
    epinephrine (adrenergic agonist)
169
Q

Nursing Implications for cholinergic drugs

A
  • These drugs will stimulate the PNS & mimic the action of acetylcholine.
  • Assess:
    Allergy, presence of GI or GU obstruction, asthma, peptic ulcer disease, & coronary artery disease
    Baseline assessment of VS, systems overview
  • Teach:
    Take meds as ordered. Never stop abruptly.
    Spread doses evenly apart to optimize the effects.
    Overdosing can cause life-threatening problems.
    Do not adjust dosages unless directed by prescriber.
  • When prescribed for Alzheimer’s disease, be honest with caregivers & clients that the drugs are for management of symptoms (not a cure).
  • Atropine is the antidote for cholinergics- Have it readily available.
  • Teach:
    Notify prescriber if client experiences:
    Muscle weakness
    Abdominal cramps, diarrhea
    Difficulty breathing
  • If post-op , w/decreased GI peristalsis, monitor for:
    Increased bowel sounds, passage of flatus, occurrence of BM
  • Monitor for therapeutic effects.
  • In clients with Alzheimer’s disease:
    Improvement in symptoms
    Improvement in mood and decrease in confusion
    Therapeutic effects of anti-Alzheimer’s drugs may not occur for up to 6 weeks
170
Q

Cholinergic-blocking drugs: MOA

A
  • Block the action of the neurotransmitter acetylcholine in PNS
  • referred to as anticholinergic drugs
  • They are competitive antagonists:
  • They compete with acetylcholine for binding at the muscarinic receptors of the PNS
  • Once bound to a receptor they inhibit cholinergic nerve transmission
171
Q

Cholinergic-blocking drugs: drug effects

A
  • Anticholinergics have the opposite effects of the cholinergic drugs!
  • Major sites of action:
    Heart
    Respiratory tract
    GI tract
    Bladder
    Eye
    Exocrine glands (sweat gland, salivary gland)
  • CV effects:
    Increased HR
  • Respiratory effects:
    Dry mucous membranes and bronchial dilation
  • GI effects:
    Decrease GI motility, GI secretions, and salivation
  • GU effects:
    Decreased bladder contraction=urinary retention
  • Skin:
    Reduce sweating
  • Eyes:
    Pupil dilation and increase intraocular pressure
172
Q

prototype: atropine

A
  • MOA: cholinergic blocker
  • Indications: primarily for CV disorders:
    Symptomatic second-degree atrioventricular block
    ACLS – for sinus bradycardia and ventricular systole
  • Contraindications:
    Angle-closure glaucoma
    Caution in patients with hepatic and renal dysfunction, GI conditions and GU conditions
  • AE’s:
  • table 21-2 Tachycardia, irritability, delirium, dilated pupils, decreased secretion and urinary retention??
    -Interactions: antacids, anticholinergics (additive effect), antihistamines, TCAs, digoxin (inc. effect of digoxin)
173
Q

Drug Effects & AE/SE: block PNS

A
  • CV:
    small doses: decrease HR
    large doses: increase HR (tachycardia)
    HTN, dysrhythmias, palpitations
  • CNS:
    small doses: decrease muscle rigidity & tremors
    large doses: drowsiness, disorientation, hallucinations
    others: excitation, restlessness, irritability, delirium, ataxia, confusion
  • Eyes:
    mydriasis (blurred vision), increased intraocular pressure
  • GI:
    decreased salivation, gastric secretions & motility (constipation)
  • GU:
    urinary retention
  • Respiratory
    decreased bronchial secretions, dilate airways
  • Glands:
    decreased sweating
174
Q

Nursing Implications forcholinergic-blocking drugs

A

Assess:
- Baseline VS
- Thorough health history & physical assessment
- Lifespan considerations: very young and/or older adult are particularly vulnerable to AE/SE- restlessness, irritability, disorientation, constipation, urinary retention, blurred vision, tachycardia
Contraindications:
- Angle-closure glaucoma
- Acute asthma or other respiratory distress
- Advanced liver or renal dysfunction, hiatal hernia associated with reflux esophagitis, intestinal atony, GI/GU obstructions, severe ulcerative colitis

175
Q

Atropine Overdose

A 
Hot as a hare (hyperthermia)
Blind as a bat (mydriasis)
Mad as a hatter (confusion, delirium)
 Red as a beet (flushed face)
Dry as a bone (decreased secretions, thirsty)
176
Q

Nursing Implications for atropine overdose

A 
- Supportive and symptomatic therapy:
hospitalized
continuous ECG monitor
activated charcoal PO or NG
- Treat shock- IV fluids
- Treat neuro changes- safety

Pharmacology (5 decks)

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