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NURS 2500 > CLASS 3 - PAIN + ANALGESICS > Flashcards

CLASS 3 - PAIN + ANALGESICS Flashcards

1
Q

What is a prototype drug?

A

One specific drug that best represents the classification of drugs. Other drugs in the classifcation are compared to the prototype bc it sets the standard for that classification of drugs.

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2
Q

What is a prodrug? Give an example.

A

A prodrug is a precursor drug that must undergo conversion in the liver to the active form. Ex - codeine is converted to morphine in the liver.

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3
Q

What is an opioid?

A

Opioid is a general term that is defined as any drug that has actions similar to morphine.

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4
Q

Define opiate.

A

The term opiate applies only to compounds present in opium.

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5
Q

What is nociception?

A

Nociception is the activation of the primary afferent nociceptors (PAN) w free nerve endings that respond to noxious (tissue-damaging) stimuli.

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6
Q

Describe the function of nociceptors. What happens if nociceptive stimuli are blocked?

A

Nociceptors function primarily to sense and transmit pain signals + promote the pain response. If nociceptive stimuli are blocked, pain is not perceived.

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7
Q

Identify 6 chemicals that activate PAN.

A

Bradykinin, Prostaglandin, Arachidonic acid, Serotonin, Substance P, and Histamine.

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8
Q

Identify the 4 Physiological Dimensions of Pain

A

Transduction, Transmission, Perception, and Modulation.

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9
Q

Describe the process of Transduction. Where does it occur?

A

Transduction - conversion of a noxious stimulus to a neuronal action potential.
Occurs at the level of the peripipheral free nerve endings (PANS).

Noxious stimuli cause cell damage with the release of sensitizing chemicals (prostaglandin, bradykinin, serotonin, substance p, histamine) which activate nociceptors and lead to the generation of APs.

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10
Q

What drugs are used to influence transduction? How do they do this?

A

NSAIDs block the action of COX enzymes which produce prostaglandin.
Local anesthetics, antiseizure drugs, and corticosteroids also block prostaglandin production.

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11
Q

What is transmission? Describe this process.

A

Transmission is the mvmt of pain impulses from the site of transduction to the brain.
The AP continues from the site of injury along peripheral nerve fibrers (A + C) to the spinal cord. From there, it undergoes processing in the dorsal horn and is then transmitted to the thalamus + cortex.

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12
Q

Identify the differences between A + C fibers in terms of pain sensation, acute or chronic pain, and myelination.

A

A FIBERS
pain sensation: pricking, sharp, well localized pain + short in duration.
acute pain.
myelinated.

C FIBERS
dull, aching, burning pain, slow onset
chronic
unmyelinated

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13
Q

Identify the 2 drugs used to influence the process of transmission. How do they work?

A

OPIOIDS - block the release of substance P

CANNABINOIDS - inhibit mast cell degranulation and response of nociceptive neurons

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14
Q

What is referred pain?

A

Referred pain occurs when the location of pain is referred from its origin to another site.

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15
Q

Describe the process of referred pain in terms of dorsal horn processing.

A

Once the nociceptive signal arrives in the CNS, it is processed within the dorsal horn of the spinal cord. This processing includes the release of neurotransmitters into the synaptic cleft. These neurotransmitters bind to receptors on nearby cell bodies and dendrites of cells that may be located elsewhere in the dorsal horn.

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16
Q

Describe the process of referred pain in terms of Wide Dynamic Range Neurons.

A

The dorsal horn of the spinal cord contains specialized cells called wide dynamic range neurons.
These neurons receive input from noxious stimuli carried by A and C fiber afferent pathways, and non-noxious stimuli from A fibers. These stimuli come from distant areas, providing a neural explanation for referred pain.
Inputs from both nociceptive fibers and A fibers converge on the wide dynamic range neuron, and when the message is transmitted to the brain, pain in the originating area of the body becomes poorly localized.

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17
Q

Describe perception.

A

Perception is the recognition of, definition of, and response to pain by the individual experiencing it. It is the conscious experience of pain.

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18
Q

In the brain, nociceptive input is perceived as ____.

A

pain.

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19
Q

Identify 3 drugs used to influence the perception of pain. How do they do this?

A

OPIOIDS: decrease the conscious experience of pain
NSAIDs: inhibit COX action
ADJUVANTS (ex - antidepressants): depends on the adjuvant

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20
Q

What is modulation?

A

Modulation involves the activation of descending pathways that exert inhibitory or facilitatory effects on the pathways that exert inhibitory or facilitatory effects on the transmission of pain.
ex - neurons in the brain stem descend to the spinal cord and release substances that inhibit nociceptive impulses.

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21
Q

Which drugs are used to influence modulation? How do they do this?

A

Tricyclic antidepressants - interfere w reuptake of serotonin + norepinephrine

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22
Q

Identify the 4 sources of pain

A

Somatic, visceral, neuropathic, and referred pain

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23
Q

What causes nociceptive pain? What is it responsive to?

A

Nociceptive pain is caused by damage to somatic or visceral tissue. It is the processing of noxious stimuli by an intact nervous system. Responsive to analgesics such as opioids and NSAIDS, or physical modalities.

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24
Q

What are some causes of nociceptive pain?

A

surgical incision, broken bone, arthritis, etc.

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25
Q

What are the 2 types of nociceptive pain?

A

Somatic + Visceral Pain.

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26
Q

Describe somatic pain.

A

Somatic pain is an aching or throbbing sensation. It is well localized and arises form bones, joints, muscles, or CT.

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27
Q

Describe visceral pain.

A

Visceral pain results from stimuli such as tumor involvement or obstruction. Arises from internal organs such as the intestines and bladder.

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28
Q

What is neuropathic pain? What does it responsive to?

A

Neuropathic pain is caused by damage to nerve cells or changes in spinal cord processing. It is an abnormal processing of sensory input as a result of injury to the PNS or CNS. Feels like burning, shooting, or stabbing.
Neuropathic pain is difficult to treat, but mgmt includes opioids, antiseizure drugs, and antidepressants.

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29
Q

What are the 2 types of neuropathic pain?

A

Centrally generated + peripherally generated

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30
Q

Describe Centrally Generated Pain.

A

Centrally generated pain is an injury to the CNS or PNS; disregulation of the ANS.

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31
Q

Describe Peripherally Generated Pain.

A

Painful polyneuropathies in which pain is felt along the distribution of many peripheral nerves (ex - diabetic neuropathy).

OR

Painful mononeuropathies usually associated w a known peripheral nerve injury and in whcih pain is felt partly along the distribution of the damaged nerve (ex - nerve root compression)

32
Q

Differentiate between acute and persistent/chronic pain in terms of the following characteristics:

  • onset
  • duration
  • severity
  • cause of pain
  • usual goals of treatment
A

ACUTE PAIN

  • sudden onset
  • duration: usually w/in the normal time for healing
  • mild-severe
  • in general, caused by precipitating illness or event (ex - surgery)
  • goal of treatment = pain control w eventual elimination

CHRONIC PAIN

  • gradual or sudden onset
  • longer than 3-6 months; may start as acute injury but continues past normal healing time
  • mild - severe
  • cause may not be known
  • goal of treatment = minimize pain as much as possible, enhanc function and QOL.
33
Q

What are the typical physical and behavioural manifestations of acute pain?

A

These manifestations reflect SNS activation

  • increased HR
  • increased RR
  • increased BP
  • diaphoresis, pallor
  • anxiety, agitation, confusion
34
Q

What are the typical physical and behavioural manifestations of chronic pain?

A

Strictly behavioural manifestations, no affect on SNS

  • changes in affect
  • decreased physical mvmt + activity
  • fatigue
  • depression, anxiety
35
Q

what is breakthrough pain?

A

moderate to severe pain that occurs despite treatment

36
Q

Define the PAIN acronym

A

Pattern (onset + duration)
Area (location)
Intensity
Nature (quality / characteristics)

37
Q

Define the OPQRSTUV acronym used for assessment

A 
Onset
Provoking / Palliative factors
Quality + Quantify Intensity
Region / Radiation
Signs + Symptoms
Timing - duration, recurrence, pattern
Understanding of cause + impact
Values of patient
38
Q

What is the preferred route of medication administration? Why?

A

Oral route. Medications are generally cheaper + maximizes patient autonomy.

39
Q

What is the WHO Analgesic Ladder?

A

The WHO analgesic ladder emphasizes that medications are administered, depending on the severity of pain, by means of a 3 step ladder approach. If pain persists or increases, medications from the next higher step are introduced to control the pain.

40
Q

Step 1 medications on the WHO ladder do not have an analgesic ceiling. What is a ceiling effect?

A

The analgesic ceiling is a dosage at which no additional analgesia is produced regardless of further dosage increases.

41
Q

Do step 3 drugs on the WHO ladder have an analgesic ceiling? What does this mean?

A

they do not. ex - dosage for morphine can go as high as needed to relieve pain.

42
Q

What are NSAIDs? How do they work? What properties do they have?

A

NSAIDs = nonsteroidal anti-inflammatory drugs. These are non-opioid analgesics.
Inhibit COX enxymes which produce prostaglandin involved in inflammation.
NSAIDs have anti-inflammatory and anti-pyretic properties.

43
Q

What are the adverse effects of NSAIDs?

A

bleeding tendencies + platelet aggregation
GI dyspepsia, ulceration, and hemorrhage
Renal insufficiency
CNS disfunction
NSAIDs (except aspirin) linked to higher risk of CV events such as MI, Stroke, and HF.

44
Q

What are selective NSAIDs? When are they used?

A

Selective NSAIDs inhibit only the COX-2 enxyme, which allows for the production of the prostaglandins that protect the stomach, while still releiving fever, pain, and inflammation. The COX-2 enzyme does not play a role in protecting the stomach or intestinal tract. Selective NSAIDs do not have the antiplatelet affects associated w non-selective NSAIDs and so do not alter clotting. Selective NSAIDs are used in cases of chronic conditions such as rheumatoid arthritis and osteoarthritis.

45
Q

What is the MOA of opioids?

A

Opioids bind to receptors (mu, kappa, or delta).

46
Q

What is an opioid agonist?

A

An opioid agonist binds to the receptors (typically mu) and causes analgesia.

Opioid agonists produce analgesia, euphoria, sedation, resp depression, and physical tolerance + dependence.

47
Q

Give some examples of opioid agonists. Which agonists have a strong efficacy? Moderate?

A

Opioid agonists include fentanyl (strong efficacy) , morphine (strong efficacy), codein (moderate efficacy), hydromorphone

48
Q

How much more potent is fentanyl than morphine?

A

100x.

49
Q

What are the 4 routes of administration of fentanyl?

A

Parenteral (surgical anesthesia)
Transdermal (patch)
Transmucosal (lozenge on stick)
Intranasal

50
Q

What % of codeine (a prodrug) converts to morphine in the liver?

A

10%

51
Q

What are the indications of codeine? How is it administered?

A

pain + cough suppression

po

52
Q

___ mg Codeine produces the same affect as ___ mg Acetaminophen

A

30 mg codeine = 325 mg acetaminophen

53
Q

What is A/Codeine? Where is this on the WHO ladder?

A

This is codeine combined with acetaminophen to form T3s. Step 2 on the WHO ladder for moderate pain.

54
Q

What is the MOA of opioid antagonists? What are their principle uses?

A

Block the effects of opioid agonists by binding to mu + kappa receptors.
Used for treatment of opioid overdoses, opioid induced constipation or respiratory depression, mgmt of opioid addiction

55
Q

Give 2 examples of an opioid antagonist

A

naloxone (reverse effects of opioid overdose)

methylnatrexone (treat opioid induced constipation).

56
Q

What is the prototype drug for pure opioid antagonists?

A

Naloxone.

57
Q

What are the 3 classes of opioid receptors?

A

Mu, Kappa, and Delta

58
Q

What is produced when Mu receptors are activated?

Kappa?

A

Mu - analgesia, respiratory depression, euphoria, sedation, and physical dependence
Kappa - analgesia and sedation

59
Q

What are the adverse effects of opioids? Which is the most common? Which 2 concerns in opioid therapy do nurses most commonly monitor for?

A
  • constipation (most common)
  • nausea + emesis
  • sedation
  • respiratory depression
  • pruritus (itching)
  • immune suppression
  • urinary retention

The 2 most common concerns in opioid therapy that nurses monitor for are secation + respiratory depression.

60
Q

What is an equianalgesic dose? When is this concept important?

A

An equianalgesic dose is a dose of one analgesis that produces pain-releiving effects equivalent to those of another analgesic.
Important when substituting one analgesic for another, when a medication is ineffective or causes intolerance

61
Q

What is the standard basis for comparison in equinalgesia?

A

10 mg parenteral morphine

62
Q

How much Morphine administered orally produces the same pain relief as 10 mg IV Morphine?

A

30 mg po

63
Q

How much Hydromorphone administered by IV produces the same pain relief as 10 mg IV morphine?

A

4 mg IV hydromorph

64
Q

What are adjuvant analgesic therapies (coanalgesics)?

How do they enhance pain tharapy?

A

Medications used in conjunction w opioid and nonopioid analgesics
ehance pain therapy through:
- enhancing effects of opioids + nonopioids
- possessing analgesic properties of their own
counteracting the adverse effects of other analgesics / treat side effects caused by opioids

65
Q

What are 3 examples of adjuvants?

A

Antidepressans
Anti-convulsants
Benzodiazepines

66
Q

What is tolerance?

A

A state in which a larger dose is required to produce the same response that could formerly be produced w/ a smaller dose. Bc of tolerance, the dosage must now be increased to maintain analgesic effects.

67
Q

What are 3 approaches to managing tolerance?

A
  • increase dosage of the analgesic
  • substitute another medication in the same class (ex morphine to oxycodone)
  • add a medication from a different drug class that will augment pain releif w/o increasing adverse effects
68
Q

What is physical dependence?

A

A client become physiologically dependent on medication. A state in which an abstinence syndrom will occur if use is abrubtly stopped.

69
Q

A client becomes physiologically dependent on an opioid medication. How can withdrawal be avoided?

A

Taper them off the drug w a careful monitoring schedule.
- Divide 24 hr dose by 2 and give 25% of this decreased amount every 6 hours.
- After 2 days, reduce this dose by a additional 25% every 2 days until the 24 hr - Oral dose is 30 mg / day.
after 2 days on the minimum dosage, the opioid is discontinued.

70
Q

Define addiction.

A

Addiction is a primary, chronic, neurological disease w genetic, psychosocial, and environmental factors influencing its development and manifestations. It is characterised by behaviours that include one or more of the following:

  • impaired control over drug use
  • compulsive use
  • continued use despite harm
  • craving
71
Q

Define FLACC

A

Face, Legs, Activity, Crying, Consolability

72
Q

Describe how you would assess pain in a paralyzed patient.

A

Check HR + BP - treat and reassess w/in one hour if you notice an increased HR + BP.
Assess pupils every hour - if they are larger in diameter than the previous hour, pain may be present.

73
Q

What is pharmacokinetics?

A

Focuses on what the body does to the drug and how drugs move through the body.

74
Q

What is pharmacodynamics?

A

Pharmacodynamics focuses on what the drug does to the body.

75
Q

What is a drug’s half-life?

A

The time it takes for the drug to drop from its maximum concentration to half of its max level; time it takes for half of the drug to leave the body.

NURS 2500 (22 decks)

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