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Pharmacology for Nurses > Exam 1 Material > Flashcards

Exam 1 Material Flashcards

1
Q

Define pharmacology

A

The study of medicine

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2
Q

Define pharmacotherapeutics

A

Using medicine to treat disease and alleviate suffering

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3
Q

Define pharmaceutics

A

The science of preparing and dispensing/sale of drugs

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4
Q

Define drugs/medications

A

Chemically produced products that elicit an effect

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5
Q

Define biologics

A

Produced naturally in animal cells, microorganisms, or the body (ex. flu vaccine) Fastest growing group of drugs

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6
Q

Define biosimilar

A

A biologic that is almost identical to an existing, FDA approved biologic medication (reference product)

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7
Q

Define complementary and alternative medicine (CAM)

A

Natural plant extracts, herbs, vitamins, minerals, dietary supplements, therapies (massage, acupuncture, PT)

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8
Q

Define therapeutic drug classification

A

What is the clinical indicator

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9
Q

Define pharmacologic drug classification

A

How the drug works within the body; its mechanism of action

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10
Q

What are the 3 different types of drug names?

A

Chemical Generic Trade

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11
Q

What is a chemical drug name?

A
  • Only one chemical name per drug; assigned
  • Usually too long and difficult to be practical
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12
Q

What is a generic drug name?

A
  • Only one generic name per drug; assigned
  • Commonly used in practice
  • Starts with a lowercase letter
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13
Q

What is a trade drug name?

A
  • Brand, proprietary name
  • May be several trade names for one drug
  • Assigned by manufacturer
  • Patient’s may know this better
  • First letter will be capitalized
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14
Q

What is bioavailability?

A
  • Physiologic ability of drug to reach target cells and produce an effect
  • Factor that can be taken into consideration when comparing generic vs brand drugs
    • Small changes can cause changes in bioavailavility
    • Some drugs you can’t substitute them without permission (immunosuppressants)
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15
Q

Prescription vs over the counter medications

A
  • Prescriptions
    • Patient education
    • Stronger dosage
    • Drug interactions are noted
    • Takes time and money
    • More expensive
  • OTC
    • Cheaper
    • Convienent
    • Patient education through pharmacologist available
    • Treat yourself
    • May not be the right drug to treat
    • Drug interactions may not be noted
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16
Q

FDA stages of approval for a new medication

A
  1. Preclinical investigation (Safety)
    1. Basic science research, lab tests on cells, animal testing
  2. Clinical investigation (Efficacy)
    1. Clinical phase trial
  3. New drug application (NDA) reviewed (Confirm)
    1. Phase III trails and animal testing may continue
  4. Postmarketing studies (Review)
    1. Continue to observe humans for adverse effects (long term)
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17
Q

What is a schedule I drug?

A

A drug with the highest abuse potential; little or no therapeutic effects

Examples: heroin, LSD, ecstacy, marijuana

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18
Q

What is a scheudle II drug?

A

A highly controlled drug

Examples: Dilaudid, fentanyl, methamphetamine, cocaine, Ritalin

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19
Q

What is a scheule III drug?

A

Medium potential for abuse

Examples: codeine, ketamine, anabolic steroids, testosterone

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20
Q

What is a schedule IV drug?

A

A drug with little abuse potential

Examples: Xanax, Valium, Versed, Tramadol

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21
Q

What is a schedule V drug?

A

Has the lowest abuse potential; some available without prescription

Examples: Lomotil, Lyrica, cough syrup with codeine

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22
Q

What is a teratogenic substance?

A

Something that has the ability to harm a developing fetus or embryo

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23
Q

Why did the FDA implement the Pregnancy and Lactation Labeling Rule (PLLR)?

A

To better inform providers, pregnant, and lactating women about the risks and benefits of taking medication. The new labeling should help assist health professionals inform patients as well as allow patients to make their own informed and educated decisions for themselves.

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24
Q

How did the pregnancy categories change?

A

Went from:

  • Pregnancy
  • Labor and Delivery
  • Nursing Mothers

To:

  • Pregnancy (includes L&D)
  • Lactating women (includes nursing)
  • Females and Males of Reproductive Potential
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25
Q

Are OTC medications included in the pregnancy label change?

A

No

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26
Q

How can medication be administered enterally?

A
  • Tablets/capsules
  • Sublingual/buccal
    • Nasogastric/gastrostomy tube
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27
Q

How can medication be administered topically?

A
  • Lotion/gel/powder
  • Inhalation
  • Instillation/irrigation
  • Transdermal
  • Ophthalmic
  • Otic
  • Nasal
  • Vaginal
    • Rectal
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28
Q

How can medication be administered parenterally?

A
  • Intradermal
  • Subcutaneous (SC/SQ)
  • Intamuscular (IM)
  • Intravenous (IV)
  • Intraosseous (IO)
  • Epidural
    • Spinal
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29
Q

What is the enteral route?

A
  • Deposits into stomach or intestines
  • Most common route for medications
    • Convenient and less costly
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30
Q

How does are medications absorbed through the enteral route?

A

Through the surfaces of the oral mucosa, somach, and intestine

  • PO - orally - goes to stomach
  • NGT - nasogastric tube (Dobhoff/Corpak) - goes to stomach through nose
  • PEG tube (percutaneous endoscopic gastrostomy tube) - goes directly to stomach
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31
Q

Why can some tablets/capsule not be crushed?

A

If they are extended release, this would cause all of the medication to be available at once rather than allow the medication to be absorbed over an extended period of time.

Could cause toxic overdose

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32
Q

What are some similarities and differences of sublingual and buccal medication administration?

A
  • Sublingual (under tongue)
    • Rich blood supply leads to rapid onset
    • Not destroyed by digestive enzymes in stomach
    • No first-pass effect
  • Buccal (between gum and cheek)
    • Absorbed more slowly than sublingual
    • Not destroyed by digestive enzymes in stomach
      • No first-pass effect
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33
Q

Describe topical medications.

A

Applied to skin or membranes of eye, ear, nose, respiratory tract, urinary tract, vagina, or rectum.

Can produce a local or system effect - local has less adverse effects.

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34
Q

Describe parenteral medications.

A
  • Invasive (invades the body)
  • Carries risk of infection
  • Medication is delieverd with a needle into skin, subcutaneous tissue, muscle vein, artery, body cavity, or organ
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35
Q

Define pharmacokinetics.

A

What the body does to the drug

  • Absorption - where will it get in?
  • Distribution - where will it go?
  • Metabolism - how is it broken down?
  • Excretion - how does it leave?
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36
Q

Define pharmacodynamics

A

What the drug does to the body

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37
Q

What affects absorption of a drug?

A
  • A dugs is absorbed from the site of administration across one or more membranes into the bloodstream
  • Factors that affect absorption include;
    • Drug formation: pill vs liquid
    • Blood flow to absorption site
    • Surface area available for absorption
    • Contact time at absorption surface
    • Drug-drug or drug-food interactions
    • Route of administration: pill vs IV
      • Absorption is 100% complete if a drug is administered IV (100% bioavailability)
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38
Q

Define bioavailabililty

A

The amount of active drug reaching systemic circulation (the bloodstream) after administration

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39
Q

Define distribution of drugs and factors that influence it

A

Transport of drugs throughout the body

Factors that affect distribution include:

  • Blood flow to body tissues
  • Lipid solubility - based on cell membranes
  • Binding to plasma proteins (albumin)
  • Anatomic barriers (brain, placenta)
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40
Q

Define metabolism of drugs and its characteristics.

A

The liver is the primary site of drug metabolism, chemically converting drugs to less active forms for removal from the body

  • The cytochrome P450 (CYP450) enzyme system is responsible for most metabolism in the liver
    • Some people have differences in this enzyme system
  • An important factor that affects metabolism is first-pass effect
  • Metabolism usually deactivates a drug
  • Metabolism ACTIVATES prodrugs
  • Additional factors affecting metabolism include:
    • Age
    • Genetics
    • Liver disease
    • Kidney disease
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41
Q

What is the first-pass effect?

A
  • Applies to medications administered orally or directly into the stomach (via a tube)
  • First-pass effect impacts the bioavailability of medications administered via the enteral route
  • If a drug has a high first-pass effect, the IV dose will be much smaller compared to the oral dose
    • Oral dose will have a less effect unless given larger quantities
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42
Q

Define excretion of a drug and some of its properties.

A
  • Drugs are primarily removed from the body by the kidneys (urine), but may also be excreted by the respiratory tract (exhalation), bile (defecation), and glands (sweating)
  • Kidneys - when there is dysfunction, the drug action can be prolonged and cause increased adverse effects
  • Respiratory - affected by diffusion and blood flow to lungs
  • Bile - more bile is recirculated back to the liver, which can lead to prolonged drug action; some bile exits through feces
    • Tends to recirculate - not excreted as quickly
  • Glands - many drugs can be excreted via breast glands
    • Some IV drugs people can taste (secreted through salivary glands)
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43
Q

Define therapeutic range.

A

Plasma concentration of drug between minimum and effective concentration and toxic concentration

*Some drugs have a much narrower therapeutic range* - CAUTION

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44
Q

Define onset

A

Time it takes after drug administration to produce a therapeutic effect

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45
Q

Define peak for a medication

A

When the medication has reached its highest concentration in the bloodstream

  • Some medications require a loading dose in order to achieve therapeutic effect in a reasonable amount of time
  • Most drugs take 4 half-lives until it reaches an effective concentration
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46
Q

Define duration of action

A

Length of time drug maintains therapeutic effect

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47
Q

Define half-life of a drug

A

Length of time for drug concentration in plasma to be decreased by half; can be affected by liver and/or kidney function

  • Medications that are taken once a day typically have a long half life
  • Medictions that have a short half-life are taken more frequently
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48
Q

Define potency of a drug

A

Drug strength at a certain dose

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49
Q

Define efficacy of a drug

A

Drug’s ability to produce a more intense response

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50
Q

Would you rather have a drug with a higher efficacy or higher potency? Why?

A

Efficacy because you want to have a drug that will give a better effect

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51
Q

What is a drug agonist?

A

A drug that binds to a receptor site and produces the same response as the natural messenger

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52
Q

What is a drug antagonist?

A

A drug that bins to a receptor site and prevents the agonist or natural messenger from binding (produces no effect by itself); “blocker”

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53
Q

Define mechanism of action (MOA)

A

How the drug produces the desired effect(s)

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54
Q

What is pharmacogenomics?

A

The study of how genetic variation affects a person’s response to drug therapy

  • Arose as a result of the Human Genome Project
  • Realized that drugs don’t work the same way for everyone (largely due to genetic differences in enzymes)
  • “The study of the genome-wide role of human variation in drug response. Pharmacogenomics also includes the application og genomic technologies in drug discovery, disposition, and function.”
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55
Q

What is precision medicine?

A

Using the right drug for the right individual for the specific disease afflicting the individual

  • Hope to predict whether a medication will be effective and prevent adverse drug reactions
  • Goal is for more specific and successful individualized treatment
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56
Q

Define genome

A

The genome of an organism encompasses all the genetic material in the cell.

In humans, this would include the 3 billion base pairs ontained in the chromosomes in the nucleus and the approximately 16,000 base pairs in the mitochondria.

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57
Q

Define pharmacogenetics

A

The study of the role of genetic variation in determining individual drug response. Generally, pharmacogenetics has been limited to the effects of one or a few genes.

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58
Q

In what ways do genes interact with drugs?

A
  • Drug metabolism: genetic variationin coding of enzymesthat metabolize drugs
    • Enzyme may inactivate an active drug, or activate a prodrug into an active agent
  • Drug transporters: genetic variation in coding of membrane transporters that move drugs in or out of cells
    • Affects pharmacokinetics
    • Can have differing effects depending on where the transporter is expressed (kidney, brain, etc)
  • Drug target: genetic variation in coding for direct target of drugs
    • Affects pharmacodynamics
    • Usually results in decreased efficacy of the drug
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59
Q

What is the most common disease that benefits from pharmacogenomics?

A

Cancer

Drugs are less likely to be a “one-size-fits all”

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60
Q

Why do grapefruit/juice don’t mix with some medications?

A

It can:

  • Block enzymes that metabolize the drug (cause too much of the drug) - most common
    • Blocks the action of CYP3A4 in the small intestine that breaks down the drugs
  • Block transporters of the drug (too little of the drug)
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61
Q

What is medication half-life? What implications does it have?

A

The amount of time it takes the body to reduce the medication by half.

If you take more of a medication before the initial dose is out of the body, the body can accumulate the drug and can cause toxicity.

Important with acetaminophen because many drugs contain this compound and accidental overdose is common.

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62
Q

6 Rights of Medication Administration

A
  • Right Patient
  • Right Medication
  • Right Dose
  • Right Time
  • Right Route
  • Right Documentation
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63
Q

What technology helps decrease medication errors?

A
  • Computerized order entry
  • Clinical decision support systems - computer recommends
  • Barcode medication administration (BCMA)
  • Smart infusion pumps
  • Medication dispensing cabinets
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64
Q

What is anaphylaxis?

A

Sever allergic reaction that can cause: tingling-senation, severe shortness of breath, swelling, decreased blood pressure, increased heart rate, uneasy feeling

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65
Q

What is angioedema?

A

Swelling of tissue unders kin (often includes tissues of the face and airway causing an airway to be put in)

Severe allergic reaction

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66
Q

What causes an allergic reaction?

A

The immune system overreacts to a foriegn substance (allergen)

It is an unexpected chemical response

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67
Q

What is Toxic Epidermal Necrolysis (TEN)?

A

A severe reaction to a medication that causes widespread erythema, necrosis, bullous detachment of epidermis and mucrous membranes.

Involves > 30% of body surface

Will begin to develop over days and continue to develop even after medication is stopped.

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68
Q

What is Steven-Johnson Syndrome (SJS)?

A

Minor form of Toxic Epidermal Necrolysis (TEN).

Involves <10% of body surface

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69
Q

What is medication compliance and what are factors that influence it?

A

Taking the medication in which it was prescribed or the directions indicate.

Factors:

  • Finances
  • Didn’t work previously
  • Transportation
  • Side effects
  • Mistrust
  • Availability
  • Forgetfulness
  • Intolerance
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70
Q

What is the Beers criteria?

A

List of potentially inappropriate medications for older adults.

Medications associated with poor outcomes (falls, confusion, mortality).

Avoided, but used when necessary - may decrease dose

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71
Q

What is a prototype drug?

A

A model drug that is used to represent a broad drug class.

Allows you to predict actions and adverse effects of other medications in the same drug class.

Not always the most widely used drug in the class.

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72
Q

What is pain?

A
  • Whatever a person says it is, existing whenever a person says it does
  • Subjective experience
  • Warns the body to avoid a potentially ganerous situation
  • Prompts individuals to seek medical attention
  • Affected by psychological and emotional processes
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73
Q

What is acute pain?

A

Starts suddently. Warning of disease or threat to the body.

Does not last longer than 6 months.

Disappears when underlying cause has been treated or is healed.

Can develop into chronic pain. Needs to be treated so this does not happen.

Examples: broken bones, labor, surgery, burns, cuts

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74
Q

What is chronic pain?

A

Pain that persists beyond healing and lasts longer than 6 months.

Can lead to depression, fear, anxiety, and anger.

Examples: back pain, cancer, arthritis, neurogenic

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75
Q

How do you assess pain?

A

There are different scales that can be used.

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76
Q

What is nociceptive pain and how do you treat it?

A

Nerve endings receive and submit pain signals to the CNS.

Responds well to traditional pain relief methods.

Two types: somatic and visceral.

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77
Q

What is somatic pain?

A

Localized; damage or injury to skin, tissues, bones, or muscles.

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78
Q

What is visceral pain?

A

Deep, dull, throbbing, generalized; damage or injury to internal organs (viscera)

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79
Q

What is neuropathic pain? What causes it? How is it treated?

A

Direct injury to the nerves.

Character of pain: shooting, burning, stabbing, pins and needles

More difficult to treat. Treatments include: antiepileptics, antidepressants, NSAIDs, Topical creams.

Caused by: shingles, diabetes, carpal tunnel, sciatic nerve pain, phantom limb pain, disc bulging.

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80
Q

What are some nonpharmacological pain relief methods?

A
  • Physical therapy
  • Art/music therapy
  • Imagery
  • Massage
  • Therapeutic touch
  • Acupuncture
  • Reiki
  • Prayer/meditation
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81
Q

What are analgesics?

A
  • Medications to relieve pain
  • Opioids (narcotics): moderate to severe pain; act within the CNS by targeting kappa and mu receptors
  • Nonopioids: act at the nociceptor level; do not work at the CNS level
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82
Q

What responses are triggered by activating the mu receptor?

A
  • Analgesia (ability to reduce pain)
  • Decreased GI motility
  • Euphoria
  • Physical dependence
  • Respiratory depression
  • Sedation
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83
Q

What reponses are triggered by activating the kappa receptor?

A
  • Analgesia (ability to reduce pain)
  • Decreased GI motility
  • Miosis (constricted pupils)
  • Sedation
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84
Q

What are opioid agaonists?

A
  • Potential to cause physical and psychological dependence
  • Powerful CNS depressants
  • Common adverse effects: respiratory depression, sedation, nausea, vomiting, constipation
  • Morphine
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85
Q

Therapeutic class of morphine

A

Opiod analgesic

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86
Q

Pharmacological class of morphine

A

Opioid analgesic

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87
Q

Indication of morphne use

A

Severe pain, pulmonary edema, chest pain with MI

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88
Q

Mechanism of action of morphine

A

Binds to mu and kappa receptors, altering perception and response to pain while producing generalized CNS depression

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89
Q

Adverse effects of morphine

A

Confusion (especially in older patients), sedation, hypotension, respiratory depression, constipation, dizziness, itching, nausea, vomiting

Can develop a tolerance over time to analgesic, sedative, and euphoric effects, and nausea

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90
Q

Interactions of morphine

A

Use of monamine oxidase inhibitors (MAOIs; antidepressants) within the past 14 days

Other sedatives, hypnotics, and alcohol

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91
Q

Would you ever give someone extended-release morphine and immediate-release morphine at the same time?

A

Yes - to someone who has chronic pain.

Want to get rid of “break-through” pain (acute pain).

Extended release may not kick in for an hour or so.

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92
Q

Would you ever give someone an opioid analgesic (such as morphine) and a nonopioid analgesic (such as acetaminophen)?

A

Yes - percoset is acetaminophen and oxycodone

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93
Q

What is a patient controlled analgesia (PCA) pump? What is its purpose?

A

Can be used IV, epidural, or SC (dosing will differ).

Typically morphine, fentanyl, or hydromorphone.

Only the patient pushes the button.

Hopefully they end up with less doses.

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94
Q

What is an opioid antagonist?

A

An opiod blocker. Prevents the effects of opioid agonists by blocking the receptor site.

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95
Q

Therapeutic class of naloxone (Narcan, Evzio)

A

Treatment of acute opioid overdose

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96
Q

Pharmacologic class of naloxone (Narcan, Evzio)

A

Opioid receptor blocker

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97
Q

Mechanism of action of naloxone (Narcan, Evzio)

A

Blocks mu and kappa receptors to reverse the effects of opioids (including CNS and respiratory depression)

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98
Q

Administration of naloxone (Narcan, Evzio)

A

IV, IM, SC, or intranasal

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99
Q

Therapeutic class of buprenorphine (Buprenex)

A

Opioid analgesic

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100
Q

Pharmacologic class of buprenorphine (Buprenex)

A

Opioid agonist/anatagonist

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101
Q

Indications of buprenorphine (Buprenex)

A

Moderate to severe pain, treatment of opioid dependence, supression of withdrawal symptoms in detoxification

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102
Q

Mechanism of action for buprenorphine (Buprenex)

A

Binds to opiate receptors, altering perception and response to pain. Partial antagonist properties.

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103
Q

What are nonsteroidal anti-inflammatory drugs (NSAIDs)?

A

Decrease pain by inhibiting inflammation and fever.

Inhibit the synthesis of prostaglandins via the cyclooxygenase (COX) pathway.

Prostaglandins are responsible for pain, inflammation, and fever.

Inhibit one or both COX enzymes that release prostaglandins.

104
Q

What are centrally acting drugs?

A

Drugs that bypass nociceptors and act directly within the brain and spinal cord (central effect).

Alternative when clients cannot take NSAIDs.

Acetaminophen (Tylenol)

105
Q

Therapeutic class of acetaminophen (Tylenol)

A

Antipyretic, nonopiod analgesic

106
Q

Pharmacologic class of acetaminophen (Tylenol)

A

Centrally acting COX inhibitor

107
Q

Indications of acetaminophen (Tylenol)

A

mild to moderate pain, fever

108
Q

MOA of acetaminophen (Tylenol)

A

Not entirely understood.

Possibly inhibits synthesis of prostaglandins (mediators for pain and fever). Does not reduce inflammation or have cardiac or gastrointestinal effects that NSAIDs are known for (irritation, blooding, ulcers)

109
Q

Contraindications of acetaminophen (Tylenol)

A

active/severe liver disease

Use with caution with: hepatic/renal disease, chronic alcohol use, malnutrition

110
Q

Adverse effects of acetaminophen (Tylenol)

A

Hepatotoxicity

111
Q

Interactions with acetaminophen (Tylenol)

A

Inhibits warfarin metabolism leading to toxic accumulation (increases bleeding risk)

112
Q

Black box warning for acetaminophen (Tylenol)

A

Severe liver injury and can cause serious allergic reactions with symptoms of angioedema, difficulty breathing, itching or rash

113
Q

Acetaminophen vs. Ibuprophen

A
  • Ibuprofen: reduces prostaglandin production by targeting active sites of COX receptors
    • Swelling due to an injury is good because it helps to immobilize the joint
    • Redness/heat to an injured area is a sign of increased blood flow to the area
    • Arachidonic acid: reacts with COX 1 and COX 2 to produce prostaglandins
  • Acetaminophen: not an anti-inflammatory
    • No idea the mechanism
114
Q

What does inflammation do?

A
  • Kills infectious agents
  • Removes cellular debris
  • Activates repair process to initiate healing
115
Q

What are some of the chemical mediators invovled in inflammation?

A
  • Histamin
  • Leukotrienes
  • Bradykinin
  • Complement
  • Prostaglandins
116
Q

What drugs treat inflammation?

A

NSAIDS: mild to moderate pain, inflammation, fever

Corticosteroids: severe inflammation

117
Q

Therapeutic class of aspirin

A

Nonopioid analgestic, NSAID, antipyretic, myocardial infarction and TIA/stroke prophylaxis

118
Q

Pharmacological class of aspirin

A

Salicylate, COX inhibitor, platelet aggregation iinhibitor

119
Q

Indications of aspirin

A

Pain, fever, inflammation, platelet aggregation inhibitor

120
Q

MOA of aspirin

A

Irreversibly inactivates cyclooxygenase (other NSAIDs are reversible inhibitors) which blocks prostaglandin synthesis

121
Q

Contraindications of aspirin

A

Children with viral illness (risk for Reyes syndrome - swelling of the brain/liver), bleeding disorders, low platelets

Use cautiously: with other anticoagulant therapy, upcoming procedures (increasing bleeding time for up to 7 days), history of GI bleed/ulcers, renal/hepatic disease, pregnancy

122
Q

Adverse effects of aspirin

A

Gastric discomfort (enteric coated available), bleeding (high doses), GI bleeding, decreased kidney function with preexisting kidney disease

123
Q

Interactions of aspirin

A

Other anticoagulants

124
Q

General overview of ibuprofen

A

Similar MOA and efficacy as aspirin.

Adverse effects: N/V, GI ulceration and bleeding.

Avoid: cients with pre-existing renal impairment.

Cautiously use: hypertension or heart failure.

Black box warning: increased risk of MI, stroke, GI bleeding

125
Q

What are corticosteroids? What do they treat?

A

Natural hormones released by adrenal cortex.

Supress inflammation by affecting release of histamine and prostaglandins.

Effective treatment for serere inflammation.

Has potentially serious side effects. Use short-termed.

126
Q

Therapeutic class of prednisone

A

Antiinflammatory

127
Q

Pharmacologic class of prednisone

A

Corticosteroid

128
Q

Indications of prednisone

A

Inflammation, autoimmune disorders, certain cancers, allergies, post-transplant

129
Q

MOA of prednisone

A

Suppression of inflammation and immune response

130
Q

Contraindications of prednisone

A

Active infection, live virus vaccines

131
Q

Adverse effects of prednisone

A

Elevated blood glucose, mood changes (increased alertness - give in the morning) , hypertension, increased susceptibility to infection (suppresses the immune system), adrenal suppression (will taper medication to help adrenals to “turn back on”)

Long-term use: gastric ulcers (often will be on pepcid), cataracts, osteoporosis, Cushing’s syndrome (elevated blood glucose, fat redistribution, muscle weakness, bruising, brittle bones)

Adverse effects are more common with high doses/long term therapy, Long term therapy must be tapered off to prevent adrenal insufficiency

132
Q

Interactions with prednisone

A

May inhibit antibody response to vaccines

133
Q

What is a fever?

A

The body’s natural defense against foreign substances; rise in temperature creates an unsuitable environment for foreign invaders.

NSAIDs and acetaminophen are used to treat fever.

134
Q

What is anesthesia? What is the difference between local and general?

A

Anesthesia: administration of medication that causes partial or total loss of sensation (reversible)

Local: sensation (and motor activity in higher concentrations) is lost to a limited part of the body, without loss of consciousness

General: loss of sensation to the entire body, usually resulting in loss of consciousness

  • Sedation and decreased anxiety
  • Lack of awareness/amnesia
  • Skeletal muscle relaxation
  • Suppression of undesirable reflexes
  • Analgesia
135
Q

What are the types of application for local anesthesia?

A
  • Topical: applied to mucous membranesl; safe unless absorbed
  • Infiltration: injected into tissues close to the surgial site
  • Nerve block: injected into tissue surrounding nerves that supply the surgical site’ blocks sensation in a large area
  • Spinal: injected into cerebrospinal fluid (CSF) to block sensation in a large area
  • Epidural: injected into the epidural space causing loss of sensation below injection site
    • Can accidentlyturn into a sprinal fit it goes in too deep
136
Q

What are the classes of local anesthetics?

A

Esters and amides.

Amides produce fewer side effects and have longer durations.

  • Esters:
    • Cocaine
    • Procaine (Novocaine)
    • Benzocaine
  • Amides:
    • Lidocaine
    • Bupivicaine
    • Ropivicaine
137
Q

MOA of local anesthetics

A

Anesthetics blocks entry of sodium ions into the cells, stopping nerve impulse conduction. This prevents sensation or pain signals from reaching the CNS (sodium channel blockers)

138
Q

Adverse effects of local anesthetics

A
  • Allergy - rare; usually related to additives
  • Early - CNS stimulation: restless, anxious
  • Late - CNS depression: confusion, drowsy, unresponsive
  • Cardiovascular - hypertension (HTN), hypotension, dysrhythmias
  • Toxicity may develop with repeated injections or accidental IV injection
139
Q

Why is epinephrine added to local anesthetics?

A

Constricts blood vessels which decreases bleeding and keeps anesthetic at the site longer (prolongs duration)

Avoid in patients with cardiovascular disease

140
Q

Therapeutic class of lidocaine (Xylocaine)

A

Local anesthetic, antiarrhythmic

141
Q

Pharmacologic class of lidocaine (Xylocaine)

A

Amide anesthetic, sodium channel blocker

142
Q

Indications of lidocaine (Xylocaine)

A

Brief medical or dental procedures, ventricular arrhythmias (IV)

143
Q

MOA of lidocaine (Xylocaine)

A

Sodium channel blocker

144
Q

What is urticaria?

A

Hives (raised, red, itchy bumps); often associated with allergic reaction

145
Q

What is pruritus?

A

Itching; often associated with dry, scaly skin, or an infestation (mites, lice)

146
Q

What is erythema?

A

Redness; signs of inflammation.

147
Q

What is an infectious skin disorder?

A

Bacterial, fungal, parasitic, and viral

148
Q

What is an inflammatory skin disorder?

A

Injury, sunburn, gland/hormone overproduction, dermatitis, psoriasis

149
Q

What is a neoplastic skin disorder?

A

Malignant skin cancers, benign neoplasms.

150
Q

What are scabicides?

A

Treatment for scabies. Kills mites which burrow under the skin and lay eggs (scabies).

151
Q

What are pediculicides?

A

Kills lice which feed on human blood and lay eggs (nits) that attach to the hair.

152
Q

Therapeutic class of permethrin (Nix)

A

Antiparasitic

153
Q

Pharmacologic class of permethrin (Nix)

A

Scabicide, pediculicide

154
Q

Indications of permethrin (Nix)

A

Lice and mites

155
Q

MOA of permethrin (Nix)

A

Causes paralysis in lice or scabies

156
Q

Adverse effects of permethrin (Nix)

A

Few systemic effects. Locally may cause pruritus, rash, tingling, burning, erythema, edema.

157
Q

Administration of permethrin (Nix)

A

Applied as cream for scabies and shampoo for lice. Nites must be removed after treatment and hair should be inspected daily for 1-2 weeks. Follow directions on packaging! Clothing/bedding/upholstery must be treated.

158
Q

What is acne?

A

Overproduction and blockage of oil glands. Inflammation results from bacterial growth within the blocked gland.

Most common skin disorder - affects 80% of people 11 to 30 at some point

159
Q

What are treatments of acne?

A

OTC: benzoyl peroxide (Clearasil), salicylic acid

Prescription: retinoids, antibiotics, oral contraceptives

160
Q

Therapeutic class of tretinoin (Retin-A): Vitamin A analog.

161
Q

Pharmacologic class of tretinoin (Retin-A): Vitamin A analog.

162
Q

Indication of tretinoin (Retin-A): Vitamin A analog

A

Mild to moderate acne, wrinkle removal, certain leukemias, and lymphomas (orphan drug status)

163
Q

MOA of tretinoin (Retin-A): Vitamin A analog

A

Decrases size and number of oil glands; exact MOA unknown

164
Q

Contraindications of tretinoin (Retin-A): Vitamin A analog

A

Pregnancy and lactation (increased risk of birth defects)

165
Q

Adverse effects of tretinoin (Retin-A): Vitamin A analog

A

Skin irritation, rash, burning/stinging, dry and peeling skin, photosensitivity; many more serious side effects when given orally

166
Q

What is dermatitis?

A

Inflammation of theskin

  • Contact dermatitis
  • Seborrheic dermatitis
  • Stasis dermatitis
  • Atopic dermatitis (eczema)
167
Q

How do you treat skin inflammation?

A

Topical corticosteroids

OTC or prescription (depends on strength)

168
Q

Adverse effects of corticosteroids on skin?

A

Thinning of skin, redness, irritation, and hypopigmentation

169
Q

Ttreatment of psoriasis

A

Topical corticosteroids - first line treament

Retinoids

Immunosuppressants, antieoplastics, and biologics

Phototherapy

170
Q

What is mydriasis?

A

Dilation of pupil

171
Q

What is miosis?

A

Constriction of pupil

172
Q

What is cycloplegia?

A

Paralysis of the ciliary muscle of the eye, resulting in a loss of accommodation (blurred vision)

Inability to constrict or dilate your pupil

173
Q

What is glaucoma?

A

Leading preventable blidness in the US.

An eye condition that cuases damage to the optic nerve and may cause irreversible vision loss. Usually associated with increased intracocular pressure (IOP)

More common in older adults

174
Q

What is open angle glaucoma?

A
  • 90% of glaucoma cases
  • IOP increases slowly; may be asymptomatic
  • Convestion in trabecular meshwork reduces outflow of aqueous humor
  • Chronic, progressive, and irreversible
  • Early diagnosis and treatment may halt progression
  • “Open angle” indicates iris does not cover trabecular meshwork
  • No pain associated with it
175
Q

What is closed angle glaucoma?

A
  • IOP suddenly increases
  • Symptoms may include “boring” eye pain, ipsilateral headache, blurred vision, halos
  • Iris blocking trabecular meshwork blocks outflow of aqueous humor
  • Ocular emergency
    • Acute pain
    • Acute pressure from blocing canal of Schlemm
  • “Closed angle” indicates iris covers trabecular meshwork
  • Can lead to irreversible blindness
    • Treatment: conventional or laser surgery
176
Q

What is the goal for glaucoma pharmacology?

A

To prevent damage to optic nerve by lowering IOP.

Increase outflow of aqueous humor via the canal of Schlemm

Decrease formation of aqueous humor by the ciliary bodies

177
Q

What drugs increase the outflow of aqueous humor?

A
  • Prostaglandins: reduce congestion in trabecular meshwork, increasing outflow of aqueous humor; first-line/preferred drug
    • Examples: latanoprost, tafluprost, travoprost (topical)
  • Cholinergics (miotics): active cholinergic receptors causing dilation of trabecular meshwork so the canal of Schlemm can drain more aqueous humor. Can cause brow headaches, myopia (near-sighted), poor vision in low light
    • Example: pilocarpine (topical)
  • Sympathomimetics (mydriatics): conversion of drug to epinephrine increase outflow of aqueous humor.
    • Example: dipivefrin (topical)
  • Many antiglaucoma medications alter pupil diameter (this itself does not change IOP, but rather is a side effect)
178
Q

What drugs decrease fomation of aqueous humor?

A
  • Beta adrenergic blockers: MOA not fully understood. Although rare, may be absorbed systemically
    • Example: timolol (topical)
  • Carbonic anhydrase inhibitors: act as a diuretic. Monnom adverse effect - photosensitivity. Contain sulfur- do not use with sulfa allergy
    • Examples: acetazolamide, dorzolamide, brinzolamide (topical or systemic)
  • Alpha2 adrenergic agonists: less commonly prescribed (many adverse effects)
    • Example: brimonidine (Alphagan)
179
Q

Therapeutic class of latanoprost (Xalatan)

A

antiglaucoma drug

180
Q

Pharmacologic class of latanoprost (Xalatan)

A

Prostaglandin analog

181
Q

Indication for latanoprost (Xalatan)

A

Open angle glaucoma, elevated IOP

182
Q

MOA of latanoprost (Xalatan)

A

Reduction of IOP by increasing outflow of aqueous humor

183
Q

Adverse effects of latanoprost (Xalatan)

A

Stinging, eye redness, sensation of foreign body in the eye, photophobia, thickened/darkened eyelashes (not-permanent), pigmentation changes of iris (permanent)

184
Q

Nursing implication of latanoprost (Xalatan)

A

Give in the evening due to adverse effects of redness/stinging sensation. Peak effect in 12 hours. No effect on pupil size. Remove contacts before administration (wait 15 min before putting them back in); wait 5 min between administration and any other opthalmic medications

185
Q

What drugs are used for eye exams?

A

Mydriatic or cycloplegic drugs are used to dilate the pupils, allowing for visualization of interior eye

186
Q

What drugs are used for ear infections?

A

Antibiotics

Topical for external ear and systemic for inner and middle ear infections

187
Q

What is peptic ulcer disease (PUD)?

A

Ulceration located in either the stomach (gastric ulcer) or small intestine (duodenal ulcer)

Associated with smoking, stress, caffeine, corticosteroids, NSAIDs, and H pylori infection, family history, and Blood type O

NSAIDs inhibit COX-1 enzume which protects the stomach lining.

188
Q

What is H. Pylori and what can it lead to?

A

It is a gram negative bacteria that is present in 50% of the population.

Responsible for a high percentage of gastric and duodenal ulcers.

Can lead to chronic gastritis (increases acid secretions, decreases bicarbonate secretion).

Can test for it by blood sample, fecal sample, breath test, or biopsy of gastric mucosa)

189
Q

What is Gastroesophageal reflux disease (GERD)?

A

Stomach acid rises into the esophagus, causing irritiation (esophagitis) and burning sensation.

Often due to poor sphincter tone and/or obesity.

Eating right before bed is not good.

190
Q

Pharmacologic treatment of PUD and GERD?

A
  • Proton-pump inhibitors (PPIs)
  • H2 receptor blockers
  • Antacids
  • Antibiotics
  • Miscellangeous drugs
  • GOAL of therapy: symptom relief, healing of ulcer, prevent recurrance
191
Q

Characteristic of proton pump inhibitors (PPIs)

A
  • Most effective durg class for decreasing acid secretion
    • Longer duration of action than H2 blockers
  • Can be used to prevent ulcers in clients taking NSAIDs or in the critically ill (stress ulcer prophylaxis; prevent GI bleeding)
  • SHOULD BE SHORT TERM
192
Q

Therapeutic class of omeprazole (Prilosec)

A

Anti-ulcer drug

193
Q

Pharmacologic class of omeprazole (Prilosec)

A

PPI - Proton Pump inhibitor

194
Q

Indications for omeprazole (Prilosec)

A

GERD, PUD, stress ulcer prophylaxis in critrically ill, hypersecretory conditions (too much gastric acid)

195
Q

MOA of omeprazole (Prilosec)

A

Irreversibly binds H+, K+ ATPase enzyme of parietal cells (which acts as a pump to release acid/protons), thereby reducing acid secretion

196
Q

Adverse effects of omeprazole (Prilosec)

A

Headache, abdominal pain, N/V, diarrhea

Long term use: osteoporosis, increased risk of c. diff infection, vitamin B12 deficiency, risk of dementia.

197
Q

Nursing implications of omeprazole (Prilosec)

A

Give 30 min before breakfast; can take several days before relief

198
Q

Characteristics of H2 receptor blockers

A
  • Histamine has several receptors
  • H1 inflammation and allergy syptoms
  • H2 gastric acid secretion
  • H2 receptor blockers decrease volume and acidity of stomach acid
  • May be available PO or IV
199
Q

Therapeutic class of famotidine (Pepcid)

A

Anti-ulcer drug

200
Q

Pharmacologic class of omeprazole (Prilosec)

A

H2 receptor blocker

201
Q

Indications of omeprazole (Prilosec)

A

GERD, PUD, stress ulcer prophylaxis, hypersecretory conditions, indigestions

202
Q

MOA of omeprazole (Prilosec)

A

H2 receptor antagonist; inhibits volume and concentration of gastric secretions

203
Q

Adverse effects of omeprazole (Prilosec)

A

Headach, dizziness

Rare: decrease WBCs, RBCs and platelets (effects bone marrow)

204
Q

Characteristics of Antacids

A
  • Alkaline substances used to quickly neutralize stomach acid (trypically contain aluminum, magnesium, or calcium)
  • Provides quick relief of heartburn smptoms but do not promote healing of ulcers
  • Quick onset
  • Monitor electrolytes if giving in high doses or over a prolonged period of time
  • Example: Calcium carbonate (Tums)
    • Also used as a calcium supplement
205
Q

Treatment for H. Pylori

A

Combination of multiple medications, typically 2 or more antibiotics and a PPI

206
Q

Differences between laxatives and stool softeners

A

Laxatives cause peristalsis of the bowel (stimulates it to move) and can pull in more water into the intestines.

Softeners cause the stool to get softer (more water) but does not give the urge to go.

207
Q

Therapeutic class of ondansetron (Zofran)

A

Antiemetic

208
Q

Pharmacologic class of ondansetron (Zofran)

A

Seratonin (5-HT3) receptor blocker

209
Q

Indications of ondansetron (Zofran)

A

N/V, prevention of chemo or radiation related N/V, post-surgical N/V

210
Q

MOA of ondansetron (Zofran)

A

Blocks serotonin receptors in the chemorecepto trigger zone and GI tract

211
Q

Adverse effects of ondansetron (Zofran)

A

Headache, constipation, diarrhea, dizziness

212
Q

Therapeutic class promethazine (Phenergan)

A

Antiemetic, antihistamin (H1 receptors)

213
Q

Pharmacologic class promethazine (Phenergan)

A

Phenothiazine

214
Q

Indications of promethazine (Phenergan)

A

N/V, motion sickness, allergy, pre-op sedation

215
Q

MOA of promethazine (Phenergan)

A

blocks the effects of histamin and has an inhibitory effect on the chemoreceptor trigger zone

216
Q

Adverse effects of promethazine (Phenergan)

A

CNS depression, confusion, prolonged QT interval

217
Q

Nursing considerations of promethazine (Phenergan)

A

Risk of severe tissue injury if medication extravasates (leaks out of the vessel causing major tissue damage) when given through peripheral IV

Preferable to give via central line or large bore IV

On Beers criteria list (more cautious with elderly population)

218
Q

What is the recommended dietary allowance (RDA)

A

Minimum amount of vitamin or mineral needed to meet nutritional requirements of a healthy adult

Populations that may need higher than usual amounts: pregnant/breastfeeding, older adults, vegetarians/vegans, infants

Populations commonly with vitamin deficiencies: kidney/liver disease, alcohol/drug dependency

219
Q

What are nephrocaps?

A

Nephrocaps are a multivitamin specifically used for clients with chronic renal disease

Clients on dialysis tend to be deficient in water soluble vitamins (poor intake, dialyzed off, restricted protein diet)

220
Q

Indications for folic acid supplement

A

Anema (due to folic acid deficiency)

Excessive alcohol use (thiamine given as well)

Malnutrition

Methotrexate toxicity (chemotherapy drug)

Pregnancy - prevent neural tube defects (spina bifida)

221
Q

What is a banana bag?

A

A banana bag is a liter of IV fluid, typically containing a multivitamin, thiamine, folic acid, and magnesium

Most often used for clients with alcoholism who are acutely intoxicated or at risk for withdrawal

The fluid is intended to replete nutritional deficiencies (ethanol interferes with folic acid and thiamine absorption)

222
Q

Therapeutic class of ferrus sulfate (Iron)

A

Antianemic

223
Q

Pharmacologic class of ferrus sulfate (Iron)

A

iron supplement

224
Q

Indications of ferrus sulfate (Iron)

A

Prevention and treatment of iron deficiency anemia

225
Q

MOA of ferrus sulfate (Iron)

A

Iron is found in hemoglobin myoglobin, and many enzymes

After entering the bloodstream, it becomes part of iron stores

226
Q

Adverse effects of ferrus sulfate (Iron)

A

GI upset, constipation, diarrhea

227
Q

Nursing implications of ferrus sulfate (Iron)

A

Best to give on an empty stomach (food decreases absorption of iron), stool will be very dark, liquid preparations may stain teeth (use straw of place drops at back of tongue)

228
Q

Characteristics of Enteral Nutrition (Tube Feed)

A
  • Administered via the GI tract, using natural digestive processes
  • Product is chosen to meet specific needs of client
  • Adverse effects - N/V, diarrhea (start slowly and titrate)
  • Situations where enteral nutrition might be needed?
    • If they can’t swallow - sedation
    • Stroke
229
Q

Characteristics of Total Parenteral Nutrition (TPN)

A
  • Nutrition is given intravenously
  • Only if GI tract cannot be used - will try for about 5 days
  • Must be given via central line
    • Due to dextrose content it will irritate veins
  • Ordered daily; ingredients and dosages may change based upon lab values
  • Additional medications may be added to bag by pharmacy (insulin, famotidine)
  • IV tubing changed daily with each new bag
  • Risks associated with TPN - infection (bacterial growth due to dextrose), gallstones, elevated glucose, osteoporosis, fatty liver
230
Q

When discussing FDA approval of an investigational medication with a client, the nurse best summarizes the process with which of the following statements?

a. “The entire approval process takes 17 years, at which time a generic form of the medication will be available.”
b. “The approval process varies by country and it would be safe to obtain the medication from another country if it is approved sooner there.”
c. “The approval process ends once the New Drug Application has been approved; long term side effects will have been discovered by this time.”
d. “The approval may take up to 12 years or longer, and post-marketing studies will extend beyond this time to determine long-term side effects.”

A

d. “The approval may take up to 12 years or longer, and post-marketing studies will extend beyond this time to determine long-term side effects.”

231
Q

A client is prescribed oxycodone (an opiod) for post-surgical pain and expresses concern that they might become addicted. The best response by the nurse is:

a. “You can adequately control your surgical pain with acetaminophen. You do not need to fill the prescription.”
b. “I will ask your physician if you can take naloxone with the oxycodone to minimize the risk of addiction.”
c. “The risk of addiction is minimized by taking the lowest effective dose, for the shortest time necessary.”
d. “You will not become addicted to opiods if you only take the medication when your pain is unbearable.”

A

c. “The risk of addiction is minimized by taking the lowest effective dose, for the shortest time necessary.”

232
Q

A client experiencing chronic cancer pain has just received OxyContin 60 mg (extended-release oxycodone) as part of his normally scheduled morning medications. He states that he is experiencing severe pain, rated as 9/10 on the pain scale, and asks for a dose of oxycodone 10 mg (immediate release). The best course of action for the nurse is to:

a. Call the provider and question why both extended and immediate release formulations are ordered
b. Administer oxycodone 10 mg, as long as enough time has lapsed since the last dose
c. Educate the client that he should wait at least 60 minutes to see if the OxyContin provides relief
d. Express concern that the client may develop an addiction if he takes both medications

A

b. Administer oxycodone 10 mg, as long as enough time has lapsed since the last dose

233
Q

Which term best describes the route of administration for an intravenous medication?

a. Enteral
b. Parenteral
c. Transdermal
d. Topical

A

b. Parenteral

234
Q

True or False? A medication administered intravenously has 100% bioavailability.

235
Q

Which statement best describes the purpose of a loading dose?

a. To convert an inactive drug to its active form
b. To test for side effects before administering a full dose
c. To change gastric acid pH for improved drug absorption
d. To quickly achieve sufficient drug level in the bloodstream

A

d. To quickly achieve sufficient drug level in the bloodstream

236
Q

Why is the patient with kidney failure at greater risk for drug toxicity?

a. The kidneys are responsible for excreting most drugs
b. The kidneys are responsible for metabolizing most drugs
c. The kidneys are responsible for binding drugs to albumin
d. The kidneys are happy beans that do not do well under stress

A

a. The kidneys are responsible for excreting most drugs

237
Q

The “first pass effect” applies to

a. Medications administered topically
b. Medications administered via the parenteral route
c. Medications administered intravenously
d. Medications administered via the enteral route

A

d. Medications administered via the enteral route

238
Q

The term “teratogenic” indicates that a substance has the ability to:

a. Alter the chemical structure of another drug
b. Harm a developing fetus or embryo
c. Detect genetic biomarkers
d. Cause physical or psychological dependence

A

b. Harm a developing fetus or embryo

239
Q

Which of the following statements is true regarding controlled substances?

a. A schedule V drug has the highest abuse potential
b. A schedule III drug is not psychologically addictive
c. A schedule II drug is more addictive than a schedule IV drug
d. Some schedule I drugs are available over-the-counter

A

c. A schedule II drug is more addictive than a schedule IV drug

240
Q

A potentially serious adverse effect of opioid analgesics is:

a. Diarrhea
b. Respiratory depression
c. Cough
d. Anxiety

A

b. Respiratory depression

241
Q

Naloxone (Narcan) is an example of an:

a. Opioid
b. Opioid agonist
c. Opioid antagonist
d. Opioid prodrug

A

c. Opioid antagonist

242
Q

The term “NSAID” stands for:

a. Nonessential active-inflammation drug
b. Normosensory analgesic inducing drug
c. Nonsteroidal anti-inflammatory drug
d. Natural setting anti-infective drug

A

c. Nonsteroidal anti-inflammatory drug

243
Q

Name three different routes of administration for drugs that are administered parenterally?

A

IO

IV

IM

SC

244
Q

Describe what it is meant by the term “medication half-life”

A

How long it takes a medication to metabolize in the body to reduce the amount of the drug in the plasma by half

245
Q

A client is prescribed oxycodone after a surgical procedure. What adverse effects will the nurse include in client education?

A

Respiratory depression, constipation, confusion, hypertension

246
Q

Acetaminophen as the potential to cause toxicity to which organ?

247
Q

What effect can corticosteroids have on serum glucose levels?

A

Increase glucose levels

248
Q

In clients who have glaucoma, increased intraocular pressure is caused by a _____ in the outflow of aqueous humor or _____ production of aqueous humor.

A

A. Decreased

B. Increased

249
Q

Drugs that cause the pupils to constrict are called:_____

250
Q

Drugs that cause the pupils to dilate are called:_____

251
Q

Drugs that cause relaxation of the ciliary muscles are called:______

A

Cycloplegics

252
Q

Vitamin A like compounds providing resistance to bacterial infection by reducing oil production and the occurrence of clogged pores are called: _____

A

anti-acne; retinoids

253
Q

What drug does NOT exert an anti-inflammatory effect?

a. Aspirin
b. Ibuprofen
c. Celecoxib (COX-2 inhibitor)
d. Acetaminophen

A

d. Acetaminophen

254
Q

Which of the following is a potentially early adverse effect from local anesthesia?

a. Hypertension
b. Myocardial infarction (heart attack)
c. Flushing
d. Restlessness or anxiety

A

c. Flushing

255
Q

The nurse understand omeprazole (Prilosec) reduces symptoms of Peptic Ulcer Disease by what mechanism?

a. Neutralizing stomach acid
b. Inhibiting secretion of gastric acid
c. Elimination of H pylori
d. Slowing peristalsis in the upper gastrointestinal tract

A

b. Inhibiting secretion of gastric acid

256
Q

Ondansetron (Zofran) is an antiemetic that belongs to which class of drugs?

a. Neurokinin receptor agonists
b. Serotonin receptor antagonists
c. Glucocorticoids
d. Phenothiazines

A

b. Serotonin receptor antagonists

257
Q

Which of the following complaints made by the client would cause the nurse to discontinue laxative therapy?

a. Dry, flaky skin
b. Mild abdominal discomfort
c. Diarrhea and cramping
d. Soft, formed stool

A

c. Diarrhea and cramping

Pharmacology for Nurses (11 decks)

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