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RD Polytechnic BScN 2nd Year Semester 1 > Pharm 251 - Quiz #2 - Final > Flashcards

Pharm 251 - Quiz #2 - Final Flashcards

1
Q

Define analgesic.

A

Medications that relieve pain without causing loss of consciousness. Also known as “Painkillers”.

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2
Q

What are some key characteristics to be aware of regarding pain?

A
  • An unpleasant sensory and emotional experience associated with actual or potential tissue damage
  • A personal and individual experience
  • Whatever the patient says it is
  • Exists when the patient says it exists
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3
Q

Define acute pain.

A

Pain that is sudden in onset, usually subsides when treated, and typically occurs over less than a 6-week period.

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4
Q

Define addiction.

A

Strong psychological or physical dependence on a drug or other psychoactive substance, usually resulting from habitual use, that is beyond normal voluntary control.

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5
Q

Define adjuvant analgesic drugs.

A

Drugs that are added for combined therapy with a primary drug and may have additive or independent analgesic properties, or both.

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6
Q

Define agonist-antagonist substances.

A

Substances that bind to a receptor and cause a partial response that is not as strong as that caused by agonists (also known as partial agonists).

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7
Q

Define analgesic ceiling effect.

A

The effect that occurs when a particular pain drug no longer effectively controls a patient’s pain despite the administration of the highest safe dosages.

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8
Q

What is the pain called that occurs between doses of pain medications?

A

Breakthrough pain

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9
Q

What is involved with central pain?

A

Pain resulting from any disorder that causes central nervous system damage.

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10
Q

What is the gate control theory?

A

A common and well-described theory of pain transmission and pain relief. It uses a gate model to explain how impulses from damaged tissues are sensed in the brain.

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11
Q

Pain that results from a disturbance of function or pathological change in a nerve.

A

Neuropathic pain

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12
Q

Pain that arises from mechanical, chemical, or thermal irritation of peripheral sensory nerves (e.g., after surgery or trauma or associated with degenerative processes). Two subtypes of nociceptive pain are visceral and somatic.

A

Nociceptive pain

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13
Q

What are two subtypes of nociceptive pain?

A
  • visceral pain
    • somatic pain
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14
Q

A large, chemically diverse group of drugs that possess analgesic, anti-inflammatory, and antipyretic activity, but are not corticosteroids.

A

Nonsteroidal anti-inflammatory drugs (NSAIDS)

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15
Q

Synthetic drugs that bind to opiate receptors to relieve pain.

A

Opioid analgesics

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16
Q

What does it mean to be opioid naive?

A

A description of patients who are receiving opioid analgesics for the first time or intermittently for a brief period of time and who therefore are not accustomed to their effects.

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17
Q

What does it mean to be opioid tolerant?

A

The opposite of opioid naive; a description of patients who have been receiving opioid analgesics (legally or otherwise) for a period of time (1 week or longer) and who are at greater risk of opioid withdrawal syndrome upon sudden discontinuation.

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18
Q

What is opioid withdrawal?

A

The signs and symptoms associated with abstinence from, withdrawal of, or dose reduction of an opioid analgesic when the body has become physically dependent on the substance.

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19
Q

Define pain.

A

An unpleasant sensory and emotional experience associated with actual or potential tissue damage.

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20
Q

The level of stimulus that results in the sensation of pain.

A

pain threshold

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21
Q

The amount of pain a patient can endure without its interfering with normal function.

A

pain tolerance

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22
Q

Define persistent pain.

A

Recurring pain that is often difficult to treat. Includes any pain lasting longer than 3 to 6 months, pain lasting longer than 1 month after healing of an acute injury, or pain that accompanies a nonhealing tissue injury. (Also referred to as chronic or long-term pain).

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23
Q

Pain experienced in an area of the body part that has been surgically or traumatically removed.

A

phantom pain

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24
Q

What is psychological dependence?

A

A pattern of compulsive use of opioids or any other addictive substance characterized by a continuous craving for the substance and the need to use it for effects other than pain relief (also called addiction).

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25
Q

Pain occurring in an area away from the organ of origin.

A

referred pain

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26
Q

A progressively decreased responsiveness to a drug, resulting in a need for a larger dose of the drug to achieve the effect originally obtained by a smaller dose.

A

Tolerance

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27
Q

Pain that results from pathology of the vascular or perivascular tissues.

A

vascular pain

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28
Q

Pain that originates from internal organs or smooth muscles.

A

Visceral pain

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29
Q

What kinds of things can lower pain tolerance?

A
  • anger
  • anxiety
  • depression
  • discomfort
  • fear
  • isolation
  • persistent pain
  • sleeplessness
    • tiredness
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30
Q

What kinds of things can increase pain tolerance?

A
  • Diversion
  • empathy
  • rest
  • sympathy
    • medications (analgesics, antianxiety drugs, antidepressants)
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31
Q

What are some ethnocultural implications regarding pain?

A
  • Pain is experienced by individuals, not by a culture
  • There are both environmental and ethnocultural variations in the pain experience
  • Recognize the effect of social determinants of health on pain experience, pain expression, and treatment access
  • Pain behaviour and report best understood in the context of social interactions
  • Be aware of communication about cultural and religious variation
    • Remain aware of ethnocultural influences on health related behaviours
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32
Q

What does pain result from physiologically?

A
  • Pain results from stimulation of sensory nerve fibres called nociceptors.
  • These receptors transmit pain signals from various body regions to the spinal cord and brain.
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33
Q

What are some important characteristics to be aware of related to pain tolerance?

A
  • Varies from person to person
  • Subjective response to pain, not a physiological function
  • Varies by attitude, personality, environment, culture, ethnicity
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34
Q

List the five distinct processes of nociceptive pain.

A
  • Transduction
  • Conduction
  • Transmission
  • Perception
  • Modulation
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35
Q

What are the three receptors believed to be involved in pain?

A
  • Mu receptors (in the dorsal horn of the spinal card; appear to plat the most crucial role)
  • Kappa receptors
    • Delta receptors
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36
Q

When the number of receptors is high, is pain sensitivity augmented or diminished?

A

Sensitivity is diminished.

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37
Q

What is involved in pain transduction?

A
  • Transformation of stimuli into electrochemical energy
  • Release of pain-medicating chemicals
  • Nociceptors
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38
Q

During pain transduction, what is released when there is tissue injury and what do they do (generally)?

A
  • Bradykinin
  • Histamine
  • Potassium
  • Prostaglandins
  • Serotonin
  • Substance P

Generally, they stimulate nerve endings, starting the pain process

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39
Q

Where is the point of spinal cord entry for nerve impulses related to pain?

A

Dorsal horn

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40
Q

What are the two types of nociceptor pain fibers?

A
  • Large-diameter, A-delta fibres, and
  • small-diameter C fibres
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41
Q

What are some important characteristics to remember regarding pain perception?

A
  • Subjective phenomenon of pain
  • Identical stimulus can evoke different pain from one individual to another
  • “How it is felt”
  • Complex behavioural, psychological, and emotional factors
  • The number of mu receptors in the dorsal horn appear to play a crucial role in pain perception and emotional well-being
  • The larger the number of mu receptors , the less pain is perceived
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42
Q

What is involved in pain modulation?

A
  • Neural activity that controls pain transmission to neurons
  • Both peripheral and central nervous systems
  • Descending pain system
  • Enkephalins and endorphins (released to fight pain and are the bodies pain killers)
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43
Q

What is the term ‘endorphin’ short for?

A

endogenous morphine

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44
Q

Why does massaging an area often reduce the pain?

A

Relates to the gate theory. Massaing an area causes large sensory A nerve fibres to inhibit impulse transmission and therefore, causes the gate to close.

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45
Q

What is patient-controlled analgesia?

A

IV route; commonly used in hospital setting; patient able to self-medicate by pressing a button on a PCA infusion pump; shown to be effective and reduce total opioid dose used; morphine sulphate and fentanyl are commonly given by PCA.

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46
Q

What are two adjuvant drugs that are used for neuropathic pain?

A
  • Amitriptyline (antidepressant)
  • Gabapentin or pregabalin (anticonvulsants)
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47
Q

What do adjuvant drugs do?

A

They assist the primary drugs in relieving pain. Adjuvant drug therapy may include NSAIDs, antidepressants, antiepileptic drugs, and corticosteroids.

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48
Q

What is allodynia?

A

Hypersensitivity or hyperalgesia to mild stimuli such as light touch or a pinprick, or the bed sheet’s on a person’s foot.

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49
Q

What are the three steps of the WHO Three-step analgesic ladder?

A

Step 1: Nonopioids with or without adjuvant medications after the pain has been identified and assessed. If pain persists or increases, treatment moves to:

Step 2: Opioids with or without nonopioids and with or without adjuvants. If pain persists or increases, management then rises to:

Step 3: Opioids indicated for moderate to severe pain, administered with or without nonopioids or adjuvant medications

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50
Q

What are opioid drugs?

A

Synthetic drugs that bind to the opiate receptors to relieve pain.

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51
Q

What are the two classifications of opioid drugs and examples of each?

A
  • Mild agonists: codeine, hydrocodone
  • Strong agonists: morphine, hydromorphone hydrochloride, oxycodone, meperidine, fentanyl, methadone
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52
Q

Why is meperidine not recommended for long-term use?

A

Because of the accumulation of a neurotoxic metabolite, normeperidine, which can cause seizures. Can cause delirium in older adults, and serotonin syndrome.

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53
Q

What is an opioid ceiling effect?

A

Drug reaches a maximum analgesic effect. Analgesia does not improve, even with higher doses.

  • Codeine phosphate
  • Pentazocine
  • Nalbuphine
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54
Q

What are the three classifications of opioid analgesics?

A
  • Agonists (Bind to an opioid pain receptor in the brain and cause an analgesic response)
  • Agonists–antagonists (Bind to a pain receptor and cause a weaker pain response than full agonists)
  • Antagonists (nonanalgesic)(Reverse the effects of these drugs on pain receptors; bind to a pain receptor and exert no response)
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55
Q

What are the Indications for opioid analgesics?

A
  • Mainly used to alleviate moderate to severe pain
  • Often first line agents analgesic in immediate post operative setting
  • Often given with adjuvant analgesic drugs to assist primary drugs with pain relief
  • Balanced anaesthesia
  • Opioids are also used for:
    • Cough centre suppression
    • Treatment of diarrhea
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56
Q

What are the contraindications for opioid analgesics?

A
  • Known drug allergy
  • Severe asthma
  • Use with extreme caution in patients with the following:
  • Respiratory insufficiency
  • Elevated intracranial pressure
  • Morbid obesity or sleep apnea
  • Paralytic ileus
  • Pregnancy
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57
Q

What are the adverse effects of opioid analgesics?

A
  • Central nervous system (CNS) depression
  • Leads to respiratory depression (Most serious adverse effect)
  • Nausea, vomiting, constipation, biliary tract spasm
  • Urinary retention
  • Hypotension, palpitations, flushing
  • Itching, rash, wheal formation
  • Pinpoint pupils indicating a possible overdose
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58
Q

What do biological response-modifying drugs do?

A

Alter the body’s response to diseases such as cancer and autoimmune, inflammatory, and infectious diseases

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59
Q

What are two types of BRM drugs?

A
  • Hematopoietic drugs
  • Immunomodulating drugs
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60
Q

What are the four categories of immunomodulating drugs?

A
  • Interferons (IFNs)
  • Monoclonal antibodies (MABs)
  • Interleukin (IL) receptor agonists and antagonists
  • Miscellaneous drugs
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61
Q

What are the main functions of immunomodulating drugs?

A
  • Medications that therapeutically alter a patient’s immune response to malignant tumour cells
  • Drugs that modify the body’s own immune response so that it can destroy various viruses and cancerous cells
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62
Q

What are the four possible components of cancer therapy?

A
  • Surgery
  • Chemotherapy
  • Radiation
  • Immunomodulating drugs
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63
Q

What other diseases is immunomodulating drugs used for?

A
  • Autoimmune disease
  • Inflammatory disease
  • Infectious disease
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64
Q

What are the mechanisms of action for biological response-modifying drugs?

A
  • Enhancement of hematopoietic function
  • Enhancement or regulation of the host’s immune system defenses against the tumour
  • Inhibition of metastases, prevention of cell division, or inhibition of cell maturation
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65
Q

Which component of the immune system is Mediated by B-cell functions (antibodies)?

A

Humoral immunity

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66
Q

Which component of the immune system is mediated by T-cell functions?

A

cell-mediated immunity

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67
Q

Define adjuvant.

A

A nonspecific immunostimulant that enhances overall immune function rather than stimulating the function of a specific immune system cell or cytokine through specific chemical reactions.

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68
Q

Define antibodies.

A

Immunoglobulins produced by lymphocytes in response to bacteria, viruses, or other antigenic substances.

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69
Q

Define antigen.

A

Substances that are capable of inducing specific immune responses and reacting with the specific products of those responses, such as antibodies and specifically sensitized T lymphocytes. Antigens can be soluble (e.g., a foreign protein) or particulate or insoluble (e.g., a bacterial cell).

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70
Q

Define autoimmune disorder.

A

A disorder that occurs when the body’s tissues are attacked by its own immune system.

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71
Q

Define B lymphocytes (B cells).

A

Leukocytes of the humoral immune system that develop into plasma cells and then produce the antibodies that bind to and inactivate antigens. B cells are one of the two principal types of lymphocytes; T lymphocytes are the other.

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72
Q

Define biological response-modifying drugs (BRMs).

A

A broad class of drugs that includes hematopoietic drugs and immunomodulating drugs; often referred to as biological response modifiers, they alter the body’s response to diseases such as cancer as well as autoimmune, inflammatory, and infectious diseases. Examples are cytokines (e.g., interleukin, interferons), monoclonal antibodies, and vaccines. They are also called biomodulators or immunomodulating drugs. Biological response–modifying drugs may be adjuvants, immunostimulants, or immunosuppressants.

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73
Q

Define cell-mediated immunity.

A

One of two major parts of the immune system. CMI consists of nonspecific immune responses mediated primarily by T lymphocytes (T cells) and other immune system cells (e.g., monocytes, macrophages, neutrophils) but not antibody-producing cells (B lymphocytes).

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74
Q

Define colony-stimulating factors.

A

Cytokines that regulate the growth, differentiation, and function of bone marrow stem cells.

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75
Q

What are cytokines?

A

Nonantibody proteins released by specific cell populations (e.g., activated T cells) on contact with antigens. Cytokines act as intercellular mediators of an immune response.

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76
Q

What is a cytotoxic T-cell?

A

Differentiated T cells that can recognize and lyse (rupture) target cells that bear foreign antigens on their surfaces; also called natural killer cells. These antigens are recognized by the corresponding antigen receptors that are expressed (displayed) on the cytotoxic T cell surface.

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77
Q

What is the process of differentiation?

A

An important part of normal cellular growth in which immature cells mature into specialized cells.

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78
Q

What are DMARDs?

A

Disease-modifying antirheumatic drugs. Medications used in the treatment of rheumatic diseases that have the potential to arrest or slow the actual disease process instead of providing only anti-inflammatory and analgesic effects.

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79
Q

What is hematopoiesis?

A

All of the body’s processes originating in the bone marrow that result in the formation of various types of blood components (adjective: hematopoietic); includes the three main processes of differentiation (see earlier): erythropoiesis (formation of red blood cells, or erythrocytes), leukopoiesis (formation of white blood cells, or leukocytes), and thrombopoiesis (formation of platelets, or thrombocytes).

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80
Q

What is humoral immunity?

A

All immune responses mediated by B cells, which ultimately work through the production of antibodies against specific antigens; humoral immunity acts in collaboration with cell-mediated immunity.

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81
Q

What are immunoglobins?

A

Proteins belonging to any of five structurally and antigenically distinct classes of antibodies present in the serum and external secretions of the body.

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82
Q

What is an immunostimulant?

A

A drug that enhances immune response through specific and nonspecific chemical interactions with particular immune system components; an example is interleukin-2.

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83
Q

What is an immunosupressant?

A

Drugs that decrease or prevent an immune response.

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84
Q

What are interferons?

A

One type of cytokine that promotes resistance to viral infections in uninfected cells and can also strengthen the body’s immune response to cancer cells.

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85
Q

What are leukocytes?

A

All subtypes of white blood cells; leukocytes include granulocytes (neutrophils, eosinophils, and basophils), monocytes, and lymphocytes (B cells and T cells); some monocytes also develop into tissue macrophages.

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86
Q

What are lymphokine-activated killer cells? (LAK cells)

A

Cytotoxic T cells that have been activated by interleukin-2 and therefore have a stronger and more specific response against cancer cells than other cytotoxic T cells.

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87
Q

What are lymphokines?

A

Cytokines that are produced by sensitized T lymphocytes on contact with antigen particles.

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88
Q

What is a memory cell?

A

Cells involved in the humoral immune system that remember the exact characteristics of a particular foreign invader or antigen for the purpose of an expediting immune response in the event of future exposure to this antigen.

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89
Q

What is monoclonal?

A

A group of identical cells or organisms derived from a single cell.

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90
Q

What are plasma cells?

A

Cells derived from B cells found in the bone marrow, connective tissue, and blood. They produce antibodies.

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91
Q

What is rheumatism?

A

Any of several disorders characterized by inflammation, degeneration, or metabolic derangement of connective tissue structures, especially joints and related structures.

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92
Q

What are T-helper cells?

A

Cells that promote and direct the actions of other cells of the immune system.

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93
Q

What are T-lymphocytes (T-cells)?

A

Leukocytes of the cell-mediated immune system; unlike B cells, they are not involved in the production of antibodies but instead occur in various cell subtypes (e.g., T helper cells, T suppressor cells, and cytotoxic T cells); they act through direct cell-to-cell contact or through production of cytokines that guide the functions of other immune system components (e.g., B cells, antibodies).

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94
Q

What are T-suppressor cells?

A

Cells that regulate and limit the immune response, balancing the effects of T helper cells.

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95
Q

What are tumour antigens?

A

Chemical compounds expressed on the surfaces of tumour cells. They signal to the immune system that these cells do not belong in the body, labelling the tumour cells as foreign.

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96
Q

What is the ratio of T-helper: T-suppressor?

A

2:1

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97
Q

What are the five major types of naturally occurring immunoglobins?

A

M (primary antibody produced after contact with antigen)

A (found in saliva, breast milk, and colostrum, secr. in GI and resp)

D (may be involved in parasitic infections)

G (main antibody - long-lasting memory)

E (mediates allergic reactions)

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98
Q

What are the 3 types of T-cells?

A
  • Cytotoxic T cells
  • T-helper cells
  • T-suppressor cells
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99
Q

True or false. Overactive T-suppressor cells may be responsible for clinically significant cancer cases by permitting tumour growth beyond immune system control.

A

True

100
Q

What are the main therapeutic effects of BRMs?

A
  • Enhancement of hematopoietic function
  • Regulation or enhancement of the immune response, including cytotoxic or cytostatic activity against cancer cells
  • Inhibition of metastases, prevention of cell division, or inhibition of cell maturation
101
Q

What do hematopoietic drugs do?

A

Promote the synthesis of various types of major blood components by promoting the growth or differentiation and the function of their precursor cells in the bone marrow

102
Q

What are two uses for hematopoietic drugs?

A
  • Decrease the duration of chemotherapy-induced anemia, neutropenia, and thrombocytopenia
  • Enable higher doses of chemotherapy to be given
103
Q

Name one erythropoietic drug.

A

darbepoetin alfa

104
Q

Name one colony-stimulating factor.

A

filgrastim

105
Q

What does the colony-stimulating factor filgrastim do?

A
  • Promotes the proliferation, differentiation, and activation of the cells that make granulocytes (primary defence against bacterial and fungal infections)
  • Prevents or treats febrile neutropenia
106
Q

What is important to know related to filgrastim relative to myelosuppressive antineoplastics?

A

Filgrastim must be taken before a patient develops an infection but not within 24 hours before or after myelosuppressive chemotherapeutic drugs.

107
Q

What is the mechanism of action of hematopoietic drugs?

A
  • Decrease the duration of chemotherapy-induced anemia, neutropenia, and thrombocytopenia
  • Allow for higher dosages of chemotherapy
  • Decrease bone marrow recovery time after bone marrow transplantation or irradiation
  • Stimulate other cells in the immune system to destroy or inhibit the growth of cancer cells, as well as virus- or fungus-infected cells
108
Q

What are some key features of filgrastim administration?

A
  • Do not start until 24hrs after chemo is completed
  • Keep refrigerated, take out minimum 30 minutes to warm up before use
  • Use abdomen or back of arms for SC location
  • Discontinue after the ANC has reached 1 x 109 / L
  • Note: Nadir is when the blood counts (mainly ANC and platelet counts) are at their lowest. Nadir could start 7-10 days post chemo and last as longs as 28 days
109
Q

What are the indications for hematopoietic drugs?

A
  • Used for patients who have experienced destruction of bone marrow cells as a result of cytotoxic chemotherapy.
  • Decrease the duration of low neutrophil counts, thus reducing the incidence and duration of infections.
  • Enhance the functioning of mature cells of the immune system, resulting in greater ability to kill cancer cells as well as virus- and fungus-infected cells.
  • Enhance red blood cell and platelet counts in patients with bone marrow suppression resulting from chemotherapy.
  • Allow higher doses of chemotherapy, resulting in the destruction of a greater number of cancer cells.
110
Q

What are the adverse effects of hematopoietic drugs?

A
  • Usually mild
  • Most common include:
    • Fever
    • Muscle aches
    • Bone pain
    • Flushing
111
Q

What are the three basic properties of interferons?

A
  • Antiviral
  • Antitumour
  • Immunomodulating
112
Q

What do interferons do?

A
  • Protect human cells from virus attack
  • Prevent cancer cells from dividing and replicating
  • Increase the activity of other immune system cells, such as macrophages, neutrophils, and NK cells
113
Q

What are the effects of interferons on the immune system?

A
  • Antiviral/Antitumor/Immune Modulator/Suppress
  • Restore the immune system’s function if it is impaired
  • Augment the immune system’s ability to function as the body’s defense
  • Inhibit the immune system from working
    • Helpful in autoimmune disorders
114
Q

What are alfa interferons used for?

A
  • Viral infections
    • Cancer
115
Q

What are beta interferons used for?

A
  • Autoimmune disorders such as multiple sclerosis
116
Q

What is the dose limiting adverse effect for interferons?

A

Fatigue

117
Q

What are common adverse effects for interferons?

A
  • Flulike effects:
    • Fever
    • Chills
    • Headache
    • Myalgia
118
Q

What are the indications for interferon alfa-2a?

A
  • chronic active hepatitis B
  • chronic Hepatitis C
  • chronic myelogenous leukemia
  • multiple myeloma
  • non-Hodgkins lymphoma
  • malignant melanoma
  • AIDS-related Kaposi sarcome
119
Q

What are the indications for peginterferon alfa-2a?

A

chronic active hepatitis B or chronic hepatitis C

120
Q

What are IFN-ß products indicated for?

A

Treatment of relapsing-remitting multiple sclerosis;

contraindicated for allergies to human albumin

121
Q

What are monoclonal antibodies used for?

A

˜For treatment of cancer, rheumatoid arthritis (RA), multiple sclerosis, and organ transplantation

122
Q

What are some advantages of monoclonal antibodies?

A
  • Specifically target cancer cells and have minimal effect on healthy cells
  • Fewer adverse effects than traditional antineoplastic medications
123
Q

Why are monoclonal antibodies contraindicated for active TB and other infections?

A

Because of their immunosuppressive qualities.

124
Q

What is tumor necrosis factor (TNF)?

A

A cytokine involved in systemic inflammation and is a member of a group of cytokines that stimulate the acute phase reaction. It is produced chiefly by activated macrophages, although it can be produced by other cell types as well

125
Q

What are TNF inhibitors used for?

A

Drugs that help stop inflammation. They’re used to treat diseases like rheumatoid arthritis (RA), juvenile arthritis, psoriatic arthritis, plaque psoriasis, ankylosing spondylitis, ulcerative colitis (UC), and Crohn’s disease. They’re also called TNF blockers, biologic therapies, or anti-TNF drugs.

126
Q

List four monoclonal antibodies (MABs).

A
  • Adalimumab
  • Infliximab
  • Rituximab
  • Natiluzumab
127
Q

What is adalimumab (Humulin) used for?

A
  • Moderate to severe rheumatoid arthritis, alone or in combination with methotrexate or other DMARDs
  • Psoriatic arthritis, ankylosing spondylitis, Crohn’s disease, ulcerative colitis, and psoriasis.
128
Q

What contraindications are there for adalimumab?

A
  • Patients with active infectious process, whether localized or infectious, acute or chronic.
129
Q

What indications are there for infliximab?

A

It is similar to adalimumab and is indicated for ankylosing spondylitis, Crohn’s disease, and rheumatoid arthritis.

130
Q

Who is infliximab contraindicated in?

A
  • Patients with severe heart failure
  • Reported cases of fatal tuberculosis and fungal infections; recommended that they are tested for latent tuberculosis before administration,
131
Q

What is Natiluzumab indicated for?

A
  • Treatment of RRMS
132
Q

What is Rituximab indicated for?

A
  • Follicular low-grade non-Hodgkin lymphoma for patients for whom previous therapy has failed
133
Q

What is recommended to be done prior to administration of Rituximab?

A

Premedication with acetaminophen and diphenhydramine hydrochloride before each infusion of the drug to reduce well-known infusion-related adverse effects.

134
Q

How does the interleukin drug aldesleukin work to fight tumors?

A
  • Antitumour action: IL-2 is produced by activated T cells in response to macrophage-“processed” antigens and secreted IL-1.
  • IL-2 derivative aldesleukin: stimulates or restores immune response
  • Aldesleukin: binds to receptor sites on T cells, which stimulates the T cells to multiply
  • Lymphokine-activated killer cells: recognize and destroy only cancer cells and ignore normal cells
135
Q

What are adverse effects of aldesleukin?

A
  • Commonly complicated by severe toxicity.
  • Caused by Capillary Leak Syndrome
  • Capillaries lose ability to retain vital colloids in the blood; these substances are “leaked” into the surrounding tissues.
  • Result: massive fluid retention
    • Respiratory distress
    • Heart failure
    • Myocardial infarction
    • Dysrhythmias
  • Reversible after IL therapy is discontinued
136
Q

What is capillary leak syndrome and what interleukin drug is it associated with?

A
  • Severe toxicity of aldesleukin therapy
  • Capillaries lose ability to retain vital colloids in the blood; these substances are “leaked” into the surrounding tissues.
  • Result: massive fluid retention
    • Respiratory distress
    • Heart failure
    • Myocardial infarction
    • Dysrhythmias

Reversible after IL therapy is discontinued

137
Q

What characteristics are there for aldesleukin (indication, contra, and admin)?

A
  • Treatment of metastatic renal cell carcinoma and metastatic melanoma
  • Contraindicated in those with organ transplants
  • Available only for injection
138
Q

What areas of the body does rheumatoid arthritis usually affect?

A

Shoulders, elbows, wrists, knees, and ankles, and it often affects the joints on both sides of the body equally.

139
Q

What do Disease-Modifying Antirheumatic Drugs (DMARDs) do?

A
  • Modify the disease of RA
  • Exhibit anti-inflammatory, antiarthritic, and immunomodulating effects
  • Inhibit the movement of various cells into an inflamed, damaged area, such as a joint
  • Slow onset of action of several weeks versus minutes to hours for NSAIDs
  • Also referred to as slow-acting antirheumatic drugs
140
Q

List two nonbiological disease modifying antirheumatic drugs.

A
  • methotrexate
  • leflunomide
141
Q

What are the characteristics of methotrexate?

A
  • First line therapy recommended by Canadian Rheumatology Association usually in a combo of two
  • Given PER WEEKLY not daily basis (oral most common)
  • Lower doses than for cancer (7.5mg – 20 mg/wk)
  • Bone marrow suppression is most common adverse effect; stomatitis may also occur fairly commonly
  • Folic acid supplement taken concurrently to lessen adverse effects
  • Onset of action 3-6weeks, half-life 3-10 hours
142
Q

List four biological disease-modifying antirheumatic drug.

A
  • adalimumab
  • etanercept
  • infliximab
  • abatacept
143
Q

How does abatacept work?

A

It is a selective co-stimulation modulator; it inhibits T-cell activation.

144
Q

How does etanercept work?

A

is an rDNA-derived TNF-blocking drug. It binds to TNF and blocks its interaction with cell surface receptors.

145
Q

How does leflunomide work?

A

It has antiproliferative, anti-inflammatory, and immunosuppressive activity.

146
Q

What are the pertinent characteristics of etanercept?

A
  • Used to treat rheumatoid arthritis (including juvenile rheumatoid arthritis) and moderate to severe chronic plaque psoriasis
  • Patients must be screened for latex allergy (some dosage forms may contain latex).
  • Onset of action: 1 to 2 weeks
  • Contraindicated in presence of active infections
    • Reactivation of hepatitis and tuberculosis has been reported.
147
Q

What are the pertinent characteristics of abatacept?

A
  • Used to treat RA
  • Caution if the patient has a history of recurrent infections or chronic obstructive pulmonary disease
  • Patients must be up to date on immunizations before starting therapy.
  • May increase risk of infections associated with live vaccines
  • May decrease response to dead or live vaccines
148
Q

What nursing implications are there for BRM drugs?

A
  • Assess for allergies, specifically allergies to egg proteins and IgG.
  • Assess for conditions that may be contraindications.
  • Assess baseline blood counts; perform cardiac, kidney, and liver studies.
  • Assess for presence of infection.
  • Follow specific guidelines for preparation and administration of drugs.
  • Monitor the patient’s response during therapy.
  • With some BRMs, treatment with opioids, antihistamines or anti-inflammatory drugs may be required for management of bone pain and chills.
  • Aniemetics used for nausea and vomiting
  • Teach patients to report signs of infection immediately.
    • Sore throat
    • Diarrhea
    • Vomiting
    • Fever of 38.1°C or higher
    • Watching for febrile neutropenia; needs urgent treatment and monitoring
  • Monitor therapeutic responses.
    • Decrease in growth of lesion or mass
    • Improved blood counts
    • Absence of infection, anemia, and hemorrhage
    • Observe for and monitor adverse effects.
  • Remember we are looking for signs of immune system triggered** or **immune system suppressed
149
Q

What is involved in opioid tolerance?

A
  • A common physiological result of chronic opioid treatment
  • State of adaptation
  • Result: larger dose is required to maintain the same level of analgesia
150
Q

What characterizes opioid psychological dependence?

A

Addiction: a pattern of compulsive drug use characterized by a continued craving for an opioid and the need to use the opioid for effects other than pain relief

151
Q

How do you manage opioid overdose and what is the cardinal symptom of it?

A

Use naloxone hydrochloride. Severe respiratory depression is the cardinal sign. Regardless of withdrawal symptoms, when a patient experiences severe respiratory depression, an opioid antagonist should be given. Naloxone has a high affinity for opioid receptors and will knock the opioids off the receptors for about 30 - 90 minutes, allowing the person to breathe again and reverse the overdose. May need to dose multiple times as it wears off.

152
Q

How quickly can opioid withdrawal symptoms occur in an opioid naive patient?

A

Within 2 weeks of starting to take opioids

153
Q

What interactions are there for opioid analgesics?

A
  • Alcohol
  • Antihistamines
  • Barbiturates
  • Benzodiazepines
  • Promethazine
  • Monoamine oxidase inhibitors
  • Others
154
Q

What are the characteristics of codeine sulphate?

A
  • Natural opiate alkaloid (Schedule I) obtained from opium
  • Less effective
  • Ceiling effect
  • More commonly used as an antitussive drug
  • Gastrointestinal (GI) disturbance
155
Q

What kind of pain is the opioid fentanyl used for and what are its routes of administration?

A
  • Synthetic opioid (Schedule I) used to treat moderate to severe pain
  • Parenteral injections, transdermal patches (Duragesic Mat®), sublingual effervescent tablet (Fentora®)
156
Q

Which one is more potent: morphine or hydromorphone?

A

Hydromorphone. It is a very potent opioid analgesic; Schedule I drug. 1 mg of intravenous (IV) or intramuscular (IM) hydromorphone is equivalent to 7 mg of morphine.

157
Q

What are the characteristics of methadone hydrochloride?

A
  • Synthetic opioid analgesic (Schedule I)
  • Opioid of choice for detoxification treatment of opioid addicts in methadone maintenance programs
  • Renewed interest in the use of methadone for chronic (e.g., neuropathic) and cancer-related pain
  • Prolonged half-life of the drug: cause of unintentional overdoses and deaths
  • Cardiac dysrhythmias
158
Q

What are the characteristics of morphine sulphate?

A
  • Naturally occurring alkaloid derived from the opium poppy
  • Drug prototype for all opioid drugs; Schedule I controlled substance
  • Indication: severe pain
  • Oral, injectable, and rectal dosage forms; also extended-release forms
159
Q

What are the characteristics of oxycodone hydrochloride?

A
  • Structured similar to morphine
  • Synthetic opioid
  • Often combined with acetaminophen (Percocet tablets: typical is 325 mg acetaminophen and 5 mg of oxycodone)
160
Q

What are the characteristics of naloxone hydrochloride?

A
  • Pure opioid antagonist
  • Drug of choice for the complete or partial reversal of opioid-induced respiratory depression
  • Indicated in cases of suspected acute opioid overdose
  • Failure of the drug to significantly reverse the effects of the presumed opioid overdose indicates that the condition may not be related to opioid overdose.
161
Q

Non-opioid analgesic that:

  • Analgesic and antipyretic effects
  • Little to no anti-inflammatory effects
  • Available over the counter (OTC) and in combination products with opioids
A

acetaminophen (Tylenol)

162
Q

What is the mechanism of action of acetaminophen?

A

Blocks pain impulses peripherally by inhibiting prostaglandin synthesis.

163
Q

What are the indications for acetaminophen?

A
  • Mild to moderate pain
  • Fever
  • Inability to take aspirin products
164
Q

What dosage maximum is currently in place for acetaminophen and what adjustment is being considered?

A
  • Maximum daily dose for healthy adults is 4 g/day, but Health Canada is considering lowering*
  • 2 000 mg for older adults and those with liver disease
  • Inadvertent excessive doses may occur when different combination drug products are taken together.
  • Be aware of the acetaminophen content of all medications taken by the patient (OTC and prescription).
165
Q

What are the contraindications and interactions for acetaminophen?

A
  • Should not be taken in the presence of following:
    • Drug allergy
    • Liver dysfunction
    • Possible liver failure
    • G6PD deficiency
  • Dangerous interactions may occur if taken with alcohol or other drugs that are hepatotoxic.
166
Q

What approach is used to manage acetaminophen toxicity and overdose?

A
  • Even though available OTC, lethal when overdosed
  • Overdose, whether intentional or resulting from chronic unintentional misuse, causes hepatic necrosis: hepatotoxicity.
  • Long-term ingestion of large doses also causes nephropathy.
  • Recommended antidote: acetylcysteine regimen
167
Q

What are the characteristics of tramadol hydrochloride?

A
  • Central acting analgesic
  • Treatment of moderate to moderately severe pain
  • Potential adverse effects: seizures (with excess dosages) and serotonin syndrome (if taken with SSRIs)
  • Frequently combined with acetaminophen (Tramacet)
168
Q

Which herbal product is used as an analgesic?

A

Feverfew

169
Q

What are the characteristics of feverfew?

A
  • Related to the marigold family
  • Anti-inflammatory properties
  • Used to treat migraine headaches, menstrual cramps, inflammation, and fever
  • May cause GI distress, altered taste, muscle stiffness, joint pain
  • May interact with aspirin and other NSAIDs, as well as anticoagulants
170
Q

What assessment is important to do prior to administering an analgesic?

A

Perform a thorough pain assessment, including pain intensity and character, onset, location, description, precipitating and relieving factors, type, remedies, and other pain treatments.

  • Level of pain is now considered a “fifth vital sign.”
  • Rate pain on a 0–10 or similar scale.
171
Q

What three hormones are secreted by the thyroid gland?

A
  • Thyroxine (T4)
  • Tri-iodothyronine (T3)
  • Calcitonin
172
Q

What are the functions of the thyroid gland?

A
  • Regulate protein, lipid and carbohydrate metabolism
  • Assist with normal growth & development
  • Control thermoregulatory centre
  • Effect cardiovascular, neuromuscular, and endocrine systems
173
Q

abnormality in the thyroid gland itself

A

primary hypothyroidism

174
Q

˜results when the pituitary gland is dysfunctional and does not secrete thyroid-stimulating hormone (TSH)

A

secondary hypothyroidism

175
Q

results when the hypothalamus gland does not secrete thyrotropin-releasing hormone, which, in turn, reduces TSH and thyroid hormone levels

A

tertiary hypothyroidism

176
Q

What is myxedema?

A
  • Hyposecretion of thyroid hormone during adulthood
  • Decreased metabolic rate, loss of mental and physical stamina, weight gain, loss of hair, firm edema, yellow dullness of the skin
177
Q

What do you call an enlargement of the thyroid gland that results from overstimulation by elevated levels of thyroid-stimulating hormone (TSH)?

A

A goiter

178
Q

What are common symptoms of hypothyroidism?

A
  • Cold intolerance
  • Unintentional weight gain
  • Depression
  • Dry, brittle hair and nails
    • Fatigue
179
Q

What is the main thyroid replacement drug?

A

˜levothyroxine (Synthroid®, Eltroxin®, Euthyrox®)ØSynthetic thyroid hormone T4

180
Q

What is the most significant adverse effect of levothyroxine/thyroid replacement drugs?

A

Cardiac dysrhythmia

181
Q

What are the main drug interactions for thyroid replacement drugs?

A
  • Enhance warfarin so reduce dose
  • Reduce efficacy of digoxin and insulin so increased dosage may be needed
182
Q

What very important things do you need to keep in mind regarding thyroid replacement drugs?

A
  • Never discontinue abruptly
  • Give same time each day to maintain consistent blood levels
    • Take in am to decrease insomnia
  • DO NOT INTERCHANGE BRANDS!
    • Brands are not equivalent in dosing and can destabilize treatment
183
Q

What diseases can cause hyperthyroidism?

A
  • Graves’ disease
  • Multinodular disease
  • Plummer’s disease (rare)•
  • Thyroid storm (induced by stress or infection)•Severe and potentially life threatening
184
Q

What are the potential symptoms of hyperthyroidism?

A
  • Diarrhea
  • Flushing
  • Increased appetite
  • Muscle weakness
  • Sleep disorders
  • Altered menstrual flow
  • Fatigue
  • Palpitations
  • Nervousness
  • Heat intolerance
  • Irritability
185
Q

What kinds of toxicity can antithyroid medication cause?

A

Liver and bone marrow toxicity

186
Q

What are possible treatments of hyperthyroidism?

A
  • Radioactive iodine (I131): works by destroying the thyroid gland “ablation”
  • Surgery to remove all or part of the thyroid gland (Lifelong thyroid hormone replacement will be needed).
  • Antithyroid drugs: thioamide derivatives
  • Radioactive iodine (iodine 131)
187
Q

What is an adverse effect of antithyroid medication?

A

leukopenia (manifested as fever, sore throat, lesions)

188
Q

How long does it take for thyroid medications to take effect?

A

It may take 3-4 weeks for thyroid drugs to take effect

189
Q

General term for any process that stops bleeding.

A

Hemostasis

190
Q

technical term for a blood clot

A

thrombus

191
Q

thrombus that moves through blood vessels

A

Embolus

192
Q

mechanism by which formed thrombi are lysed to prevent excessive clot formation and blood vessel blockage

A

Fibrinolysis

193
Q

What does the fibrinolytic system do?

A

˜Initiates the breakdown of clots and serves to balance the clotting process

194
Q

What is the enzymatic protein called that eventually breaks down the fibrin thrombus into fibrin degradation products?

A

Plasmin

195
Q

What is the name of a rare genetic disorder where natural coagulation and hemostasis factors are limited or absent?

A

Hemophilia

196
Q

In hemophilia, what two types inhibit platelet aggregation?

A
  • Factor VII deficiency
  • Factor VIII deficiency or factor IX deficiency, or both
197
Q

As a class, what do anticoagulants do?

A
  • Inhibit the action or formation of clotting factors
  • Prevent clot formation
198
Q

As a class, what do antiplatelets do?

A
  • Inhibit platelet aggregation
  • Prevent platelet plugs
199
Q

As a class, what do Hemorheological drugs

do?

A

ØAlter platelet function without preventing the platelets from working

200
Q

What do thrombolytic drugs do?

A

Lyse (breakdown) existing clots

201
Q

What do antifibrinolytic or hemostatic drugs do?

A

Promote blood coagulation

202
Q

True or false: Anticoagulants have no direct effect on a blood clot that is already formed.

A

True. ˜Prevent intravascular thrombosis by decreasing blood coagulability˜Used prophylactically to prevent:

ØClot formation (thrombus)

ØAn embolus (dislodged clot)

203
Q

An embolus lodged in a coronary artery causes _____________.

A

myocardial infarction

204
Q

An embolism that obstructs a brain vessel can cause a _____________.

A

stroke

205
Q

An embolism that travels to the lungs is called a _____________.

A

Pulmonary embolism

206
Q

An embolism that travels to a vein is called __________________.

A

Deep vein thrombosis.

207
Q

What lab value is frequently monitored for patients receiving heparin?

A

aPTT

208
Q

True or false. A patient on LMWH requires frequent laboratory monitoring of bleeding times using tests such as aPTT.

A

False; this is not needed.

209
Q

What are the indications for heparin?

A
  • Prevent clot formation for circumstance that may lead to stroke, heart attack, pulmonary embolism, DVT
  • Also used (both heparin & LMWs) as bridge therapy when a patient stops warfarin for surgery or other invasive procedures
210
Q

What is the mode of action of warfarin.

A
  • Inhibits vitamin K synthesis by bacteria in the gastrointestinal tract
  • Action: inhibit vitamin K–dependent clotting factors II, VII, IX, and X which are normally synthesized in the liver
  • Final effect is the prevention of clot formation
211
Q

What is type 1 heparin-induced thrombocytopenia?

A
  • Gradual reduction in platelets
    • Heparin therapy can generally be continued.
212
Q

What is type 2 heparin-induced thrombocytopenia?

A
  • Acute fall in the number of platelets (more than 50% reduction from baseline)
  • Discontinue heparin therapy.
213
Q

What lab values must be monitored closely with warfarin?

A

Careful monitoring of the prothrombin time(PT)/international normalized ratio (INR)

214
Q

What is a normal INR without warfarin and a therapeutic INR with warfarin?

A

A normal INR (without warfarin) is 0.8 to 1.2, but a therapeutic INR (with warfarin) ranges from 2 to 3.5, depending on the indication for use of the drug (e.g., atrial fibrillation, thromboprevention, prosthetic heart valve).

215
Q

What is aspirin often used for and in what dosage?

A

ØUsed for stroke prevention (you have seen low dose therapy of 81mg ECASA daily)

216
Q

What is the antiplatelet drug clopidogrel indicated for?

A
  • Shown to be better than aspirin at reducing number of MI’s, strokes and vascular deaths for at-risk patients* see notes section
  • Used for above issues plus preventing TIAs and post MI thrombotic prevention
217
Q

What is Eptifibatide (Integrilin) indicated for?

A

Used to treat acute unstable angina, MI and during PCI (pericoronary interventions such as angioplasty)

218
Q

What are some important nursing implications regarding heparin administration?

A
  • Intravenous doses are usually double-checked with another nurse.
  • Ensure that subcutaneous doses are given subcutaneously, not intramuscularly.
  • Subcutaneous doses should be given in areas of deep subcutaneous fat, and sites should be rotated.
219
Q

Why shouldn’t you aspirate subcutaneous injections or massage the injection site during heparin administration?

A

ØMay cause hematoma formation

220
Q

Which herbal products have potential interactions with warfarin?

A
  • Capsicum pepper
  • Garlic
  • Ginger
  • Ginkgo
  • St. John’s wort
  • Feverfew
221
Q

What are the three most common medication incidents that occur in Canadian hospitals?

A
  • insulin
  • hydromorphone hydrochloride
    • heparin
222
Q

What is the most common contributing factor to medication errors?

A
  • Distraction and interruptions during the act of medication administration.
223
Q

What is a just culture?

A
  • Recognizes that systems are generally at fault when error occurs
    • Need for accountability
    • Remediation of
      • Workplace culture
      • Reporting structure
      • Management behaviour
    • When professionals do not follow policies or have repeated errors
      • Need for accountability
      • Remedial education
224
Q

Define adverse drug event

A

A general term that encompasses all types of clinical problems resulting from medication use.

225
Q

What drugs are commonly involved in severe medication errors?

A
  • central nervous system drugs
  • anticoagulants
  • chemotherapeutic drugs
226
Q

What is one strategy to differentiate similar drug names?

A

TALLman lettering

227
Q

While MEs can occur at any step in the medication process, which steps most commonly have errors?

A
  • Prescribing
  • Administering
  • Dispensing
  • Transcription
228
Q

What are some main issues that contribute to medication errors?

A
  • Organizational issues
  • Educational system issues
  • Sociological factors
  • Abbreviations
229
Q

List the different types of medication errors.

A
  • Near miss
    • Did not reach the patient
    • Results in no harm
  • No harm event
    • Reaches patient
    • Results in no harm
  • Medication Error
    • Causes harm
  • Critical Incident
    • Results in serious harm
230
Q

What are some key ways to prevent medication errors?

A
  • Multiple systems of checks and balances should be implemented to prevent medication errors.
  • Prescribers must write legible orders that contain correct information, or orders should be entered electronically.
  • Authoritative resources such as pharmacists or current (within the past 3 to 5 years) drug references or literature must be consulted.
  • Nurses need to always check the medication order three times before giving the drug.
  • Faculty members should not be the student’s research source regarding medications.
  • The rights of medication administration should be used consistently.
231
Q

What is involved in medication administration?

A

Continuous assessment and updating of patient medication information:

  • Verification
  • Clarification
  • Reconciliation
232
Q

What does medication reconciliation require?

A

A best possible medication history

233
Q

When should medication reconciliation take place?

A
  • At entry into the facility
  • Upon transfer from surgery
  • Into or out of the intensive care unit
  • At discharge
234
Q

What are the different categories of lipoproteins?

A
  • Very-low-density lipoprotein
    • Produced by the liver
    • Transports endogenous lipids to peripheral cells
  • Intermediate-density lipoprotein
  • Low-density lipoprotein (LDL)
  • High-density lipoprotein (HDL)
    • Responsible for “recycling” of cholesterol
    • Also known as “good cholesterol”
235
Q

List the established classes of antilipemic drugs.

A
  • Hydroxymethylglutaryl–coenzyme A (HMG–CoA) reductase inhibitors (statins)
  • Bile acid sequestrants
  • B vitamin niacin (vitamin B3, nicotinic acid)
  • Fibric acid derivatives (fibrates)
  • Cholesterol absorption inhibitor (Ezetrol®)
236
Q

Which antilipemic has the following characteristics:

  • First-line therapy for hypercholesterolemia
  • Treatment of type IIa and IIb
  • Reduces plasma concentrations of LDL cholesterol by 30 to 40%
  • Decrease in plasma triglycerides by 10 to 30%
  • Increase in HDL cholesterol by 2 to 15%ØDose dependent

Statins

A
237
Q

What is the mechanism of action for HMG-CoA Reductase Inhibitors?

A
  • Lower blood cholesterol levels by decrease rate of production
  • When less cholesterol is produced, the liver increases the number LDL receptors to recycle LDL from circulation
    • Needed for synthesis of steroids, bile, cell membranes
238
Q

What is rhabdomyolysis?

A
  • Breakdown of muscle protein
  • Myoglobinuria: urinary elimination of the muscle protein myoglobin
  • Can lead to acute kidney injury and even death
  • When recognized reasonably early, rhabdomyolysis is usually reversible with discontinuation of the statin drug.
  • Instruct patients to immediately report any signs of toxicity, including muscle soreness or changes in urine colour (tea-coloured).
239
Q

What are the main drug interactions with HMG-CoA Reductase Inhibitors?

A
  • Oral anticoagulants
  • Drugs metabolized by CYP3A4
240
Q

When are atorvastatin calcium (Lipitor®) and rosuvastatin (Crestor®) (HMG-CoA Reductase Inhibitors) usually taken?

A

Dosed once daily, usually with the evening meal or at bedtime to correlate with diurnal rhythm

241
Q

What is the mechanism of action for bile acid sequestrants?

A
  • Prevent resorption of bile acids from small intestine
  • Bile acids are necessary for absorption
    of cholesterol.
  • The more the bile acids are excreted, the more the liver converts cholesterol to bile acids, reducing cholesterol in liver and circulation
  • Commonly used as an adjunct to statin therapy
242
Q

What is an important consideration regarding drug interactions for bile acid sequestrants?

A
  • All drugs must be taken at least 1 hour before or 4 to 6 hours after the administration of bile acid sequestrants.
  • High doses of a bile acid sequestrant decrease the absorption of fat-soluble vitamins (A, D, E, and K).
243
Q

What makes niacin a unique antilipemic drug?

A

It is also a vitamin (B3)

  • Lipid-lowering properties require much higher doses than when used as a vitamin.
  • Effective, inexpensive, often used in combination with other lipid-lowering drugs
  • Often given as adjunct to statins
244
Q

What is the mechanism of action of fibric acid derivatives?

A
  • Believed to work by activating lipoprotein lipase, which breaks down cholesterol
  • Also suppress the release of free fatty acid from adipose tissue, inhibit the synthesis of triglycerides in the liver, and increase the secretion of cholesterol in the bile
245
Q

What is the mechanism of action of cholesterol absorption inhibitors?

A
  • Inhibits absorption of cholesterol and related sterols from the small intestine
  • Results in reduced total cholesterol, LDL cholesterol, apolipoprotein B, and triglyceride levels
  • Also increases HDL cholesterol levels
  • Often combined with a statin drug
  • Can be used as monotherapy
246
Q

What can be done to minimize flushing related to niacin use?

A

Small doses of aspirin or NSAIDs may be taken 30 minutes before niacin to minimize cutaneous flushing

RD Polytechnic BScN 2nd Year Semester 1 (9 decks)

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