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Physiology & Pharmacology > Pain Medications > Flashcards

Pain Medications Flashcards

1
Q

Example of Nonopioids

A

Acetaminophen NSAIDS - Ibuprofen - Aspirin - Naproxen COX-2 Inhibitors -Celecoxib

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2
Q

This class of drugs contains Aspirin…..

A

Cyclooxygenase Inhibitors

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3
Q

Cyclooxygenase class of drugs is useful for…………

A

suppressing inflammation, relieving pain and reducing fever

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4
Q

Aspirin is special within the Cyclooxygenase class because it is the only drug that can protect against

A

Myocardial Infarction and Stroke

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5
Q

Effects of Cyclooxygenase drugs are primarily achieved through

A

inhibition of cyclooxygenase enzyme

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6
Q

What is the cyclooxygenase enzyme responsible for ?

A

Synthesis of Prostanoids (Prostaglandins and other related compounds)

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7
Q

Principal Adverse effects of Cyclooxygenase Inhibitors

A

Gastric ulceration, bleeding, renal impairment MI and stroke too (except for Aspirin)

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8
Q

COX

A

Cyclooxygenase

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9
Q

Two Forms of Cyclooxygenase

A

cyclooxygenase-1 (COX -1) and cyclooxygenase- 2 (COX -2)

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10
Q

COX-1 functions

A

found in practically all tissues where it mediates “housekeeping chores” protection of gastric mucosa supporting renal function promoting platelet aggregation

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11
Q

COX-2 functions

A

produced mainly at sites of tissue injury where it mediates inflammation and sensitizes receptors to painful stimuli present in the brain where it mediates fever and contributes to perception of pain present in kidneys where it supports renal function, blood vessels where it promotes renal dilation and the colon where it can contribute to colon cancer

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12
Q

Because COX-1 primarily mediates beneficial processes, it is labeled as the

A

“good COX”

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13
Q

Because COX-2 primarily mediates harmful processes, it is labeled as the

A

“bad COX”

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14
Q

Inhibition of COX-1 (good COX) largely has what kind of effects ?

A

harmful effects gastric erosion and ulceration bleeding tendencies renal impairment

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15
Q

Inhibition of COX-1 has one very beneficial effect - what is it ?

A

Think about Aspirin - it protects against MI and stroke, secondary to reduced platelet aggregation

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16
Q

Inhibition of COX 2 largely has what kind of effects

A

beneficial effects pain alleviation suppression of inflammation reduction of fever protection against colorectal cancer

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17
Q

Two adverse effects of COX-2 Inhibition

A

renal impairment promotion of MI and stroke

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18
Q

Two Categories of Cyclooxygenase Inhibitors

A

drugs that have anti inflammatory properties and drugs that lack anti inflammatory properties

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19
Q

NSAIDS are part of which Cyclooxygenase Inhibitor category?

A

Drugs that have anti inflammatory properties

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20
Q

NSAIDS include ………….

A

Aspirin, Ibuprofen [Advil, Motrin, others], naproxen [Aleve, others] Celecoxib (Celebrex)

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21
Q

Acetaminophen is part of which Cyclooxygenase inhibitor category ?

A

Those that lack anti inflammatory properties

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22
Q

Acetaminophen includes

A

Tylenol and others

23
Q

Acetaminophen can reduce _____________ and ___________ but cannot suppress what ?

A

pain; fever It cannot suppress inflammation

24
Q

NSAIDS can be divided into two groups which are

A

first generation NSAIDS and second generation NSAIDS `

25
Q

First generation NSAIDS inhibit

A

COX-1 and COX-2

26
Q

Second Generation NSAIDS inhibit

A

COX-2 only

27
Q

Acetaminophen MOA

A

inhibits Cyclooxygenase , but not an anti inflammatory

28
Q

Acetaminophen uses

A

reduces pain and fever

29
Q

Acetaminophen Absorption

A

Rapid and nearly complete in the small intestine Depends on the rate of gastric emptying

30
Q

Acetaminophen Distribution

A

Widely distributed in body fluids except fat 10-25% protein bound

31
Q

Acetaminophen Metabolism & Excretion

A

Hepatic metabolism by cytochrome P450 enzyme. Renal excretion

32
Q

Acetaminophen RN Considerations

A

Narrow therapeutic range. Reduced maximum dose now 3600mg/day. Beware of other meds that contain acetaminophen (e.g. Vicodin, Percocet, Darvocet, Lortab, etc.) Overdose: hepatotoxicity. Side Effects: Contraindications: liver failure, >2-3 alcoholic drinks a day

33
Q

Ibuprofen MOA

A

Inhibit prostaglandins by blocking cyclooxygenase

34
Q

Ibuprofen uses

A

Anti-inflammatory, anti-pyretic, analgesic

35
Q

Ibuprofen Absorption

A

Primarily GI tract (80%) Tablets 120 minutes to peak serum concentration

36
Q

Ibuprofen Distribution

A

90-99% protein bound

37
Q

Ibuprofen Metabolism & Excretion

A

Hepatic metabolization by cytochrome P450 enzyme Excreted renally

38
Q

Ibuprofen RN Considerations

A

Overdose: Side Effects: gastrointestinal bleed (GIB), inhibits platelet aggregation, renal dysfunction Contraindications: peptic ulcer disease and chronic kidney disease (CKD)

39
Q

What are the endogenous opioid peptides found in the CNS and peripheral tissues ?

A

Endorphins, dynorphins, enkephalins. These play a role in the modulation phase of nociceptive pain. They block the pain signal’s pathway, thus decreasing the intensity of the pain

40
Q

What are the three main classes of opioid receptors ?

A

Mu, Kappa, Delta receptors

41
Q

Opioid analgesics act primarily by activating what kind of opioid receptors ?

A

Mu receptors

42
Q

The activation of mu receptors causes ……………..

A

Activation of mu receptors causes analgesia, respiratory depression, euphoria, and sedation, constipation.

43
Q

Mu receptors are also related to …………….

A

physical dependence

44
Q

The activation of kappa receptors can also produce …………..

A

analgesia and sedation

45
Q

Morphine is a ……………

A

opioid agonist

46
Q

Morphine MOA

A

Works directly on the CNS by mimicking the actions of endogenous opioid peptides, primarily at mu and partly at kappa opioid receptors

47
Q

Morphine uses

A

pain, cough, dyspnea

48
Q

Morphine Absorption

A

30mg PO = 10mg IV PO, 50% bioavailable, plasma levels peak in 30 minutes IV, 100% bioavailable, plasma levels peak in 20 minutes 40% protein bound

49
Q

Morphine Distribution

A

skeletal muscle, kidneys, liver, intestinal tract, lungs, spleen and brain. Morphine also crosses the placental membranes and has been found in breast milk.

50
Q

Morphine Metabolism & Excretion

A

Liver, first pass effect Metabolites (morphine 3- and 6-glucouronides) can accumulate in renal failure and cause toxicity. Renal excretion 90%, biliary 10%

51
Q

Morphine RN Considerations

A

Overdose: Respiratory Depression Anticipate constipation and treat preemptively

52
Q

Non pharmacologic pain relief

A

Positioning: Immobilization Cutaneous stimulation: Heat Cold Massage Quiet Music therapy Distraction: Humor Relaxation using the patient’s own memory of peaceful events Eliciting the physiologic Relaxation Response

53
Q

Barriers to Pain Management

A

Lack of education Importance of recognizing and addressing barriers Specific barriers: Inadequate assessment Cognition of client Fear of side effects Fear of addiction/tolerance Fear of respiratory depression Fear of hastening death Healthcare systems Cost and reimbursement

54
Q

What is the WHO pain ladder

A

Guidelines based on pain ratings for the type and combination of analgesics administered

  • *Pain Level 1-3/10**
  • Non Opioid +/- adjuvant*
  • *Pain Level 4-6/10**

Weak opioid for mild to moderate pain +/- nonopioid +/-adjuvant

Pain level 7-10/10

  • Strong opioid for moderate to severe pain (morphine)*
  • +/- non opioid +/- adjuvant*

Physiology & Pharmacology (13 decks)

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