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UM - Pharmacology > Medications to treat pain and inflammation > Flashcards

Medications to treat pain and inflammation Flashcards

Opioids, NSAIDs and Acetaminophen, RA and OA drugs

1
Q

What is the role physical therapists can play in combatting the opioid epidemic

A

Patient education on use and looking out for side effects

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2
Q

List the different types of pain

A

Nociceptive
Neuropathic
Inflammatory
Non-inflammatory/non-neuropathic

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3
Q

What is nociceptive pain

A

Somatic - well localized (lots of receptors) in soft tissue and bone
Visceral - diffuse and vague - hollow organs and blood vessels

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4
Q

What is neuropathic pain

A

Pain to Brain, SC, or peripheral nerves as tingling, burning or electrical

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5
Q

What is inflammatory pain

A

Inflammatory markers cause local damage to tissue and lead to nociceptive pain

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6
Q

What is non-inflammatory/non-neuropathic pain

A

Wide spread pain with no definitive tissue or no known injury

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7
Q

What types of pain medications should be given for:

Nociceptive pain

A
  • mild to moderate: acetaminophen, NSAIDs

- moderate to severe: opioids

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8
Q

What types of pain medications should be given for:

neuropathic pain

A

Antidepressants, antiseizure

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9
Q

What types of pain medications should be given for:

Inflammatory

A

NSAIDs & other medications to decrease inflammation

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10
Q

What types of pain medications should be given for:

Noninflammatory/nonneuropathic pain

A

NSAIDs, acetaminophen & other modalities

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11
Q

What are the three families of endogenous opioids

A

Endorphins
Enkephalins
Dynorphins

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12
Q

Where are the opioid receptors located

A

In the CNS and the peripheral tissue

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13
Q

List the 3 types of opioid receptors

A

Mu
Kappa
Delta

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14
Q

What is the primary therapeutic effect for the opioid receptors:
Mu
Kappa
Delta

A

Spinal and Supra spinal analgesia for all 3

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15
Q

T or F: there are different categories of opioids

A

True: agonists, antagonists, and mixed agonist-antagonists

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16
Q

Strong agonist (opioids)

A

Used to treat severe pain and have a high affinity for the Mu receptor

Ex) fentanyl, hydromprpjone, meperidine, methadone, morphine (MS Cotin)

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17
Q

Mild to moderate agonists (opioids)

A

Stimulate the opioid receptors (Mu) but do not have as high affinity or efficacy as the strong agonists and are more effective at treating moderate pain

Ex) codeine

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18
Q

Mixed agonist-antagonists (opioids)

- what do they bind to

A

Most bind to Kappa as AGONIST and Mu as ANTAGONIST

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19
Q

Mixed agonists-antagonist

- function

A

Produce adequate analgesia with less risk of side effects (reduced risk of OD compared to Mu agonists but increased psychotropic effects)

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20
Q

Antagonists (opioids)

A

Used to treat addiction and overdose since they bind to all opioid receptors (w/higher affinity for Mu)
- do not produce analgesia
Ex) naloxone (Narcan)

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21
Q

Physical therapy and Naloxone Availability

A

Made available in 2019 by the APTA house of delegates

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22
Q

What is the preferred route for opioids

A

Oral

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23
Q

What are the different ways to administer opioids

A 
Oral 
Rectal (if N/V)
IV (slowly)
IM
SQ
Intrathecal
Transdermal - avoid GI and constipation 
Iontophoresis
Lozenges
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24
Q

What is the PCA

A

An IV set up that allows patients to self-administer a pre-set dose (demand dose) and has a lockout interval so patients have to wait for the next dose. First dose is the loading dose and it is larger than the demand to get desired plasma concentration established.

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25
Q

What are the 3 options for administration of PCA

A

IV - most common
Epidural PCA - directly into epidural space
Regional PCA - directly into a joint, near a peripheral nerve or into a wound (no systemic effects)

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26
Q

Why is PCA a good option?

A

Maintains drug levels within a well-defined therapeutic window

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27
Q

What are the potential problems with PCA

A 
Operating errors (misprogramming, misplacing the key)
Patient errors (lack of comprehension)
Mechanical problems (failure to deliver on demand, malfunctions)
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28
Q

Where are opioids metabolized and eliminated

A

Liver metabolized

Kidneys eliminated

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29
Q

What is the mechanism of action for opioids

A

They act on neuronal receptors in the SC (decrease ascending pain pathway) brain (increase activity of decreased pain pathway), and periphery (decrease excitability of sensory nerves) at the same time

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30
Q

What do opioid G proteins act on

A
  • Calcium channels (decrease entry & decrease NT)
  • K+ channels (loss of K to hyperpolarize mem & cause more exit K+)
    Intracellular signal pathways (inhibit - CAMP so can’t excite me round to transmit painful impulses)
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31
Q

True or false : opioids eliminate pain

A

False - they alter the perception of the pain causing a floating or euphoric feeling

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32
Q

What kind of pain are opioids good for

A

Constant moderate to severe pain (acute or chronic - cancer and sickle cell anemia but NOT msk pain)

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33
Q

How do you dose opioids

A
  1. Start with mild agonists orally
  2. Stronger agonists orally
  3. Stronger agonists parenterally
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34
Q

How can you ensure oral administration of opioids is most effective

A

Take it at on a regular schedule, not when you need it because otherwise it takes 20-30 minutes to kick in

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35
Q

Adverse effects of opioids

A
  • sedative properties
  • respiratory depression
  • postural hypotension
  • GI Distress (N/V)
  • Constipation
  • urinary retention
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36
Q

Rehab concerns with opioids

A

Want therapy to be at peak effects, but be cautious as it is also peak for side effects (monitor alertness, RR, and BP)

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37
Q

Define addiction

A

An individual repeatedly ingests certain substances for mood-altering and pleasurable experiences (different than tolerance and physical dependence) that had a psychological and psychiatric component

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38
Q

Define drug misuse

A

Use of a drug that falls outside of its intended purpose (taking a second sleeping pill, using a strong opioid for a mild ailment)

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39
Q

Define drug abuse

A

Prolonged tendency to seek out drugs that result in negative consequences (take more opioids than recommended to get “high”, take opioids without a prescription)

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40
Q

Define tolerance

A

The need to progressively increase the dosage of a drug to achieve a therapeutic effect when the drug is used for prolonged periods from receptor downregulation and desensitization

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41
Q

Tolerance & Opioids

1) when does it begin
2) when do you have to increase dose
3) how long does it last

A

1) behind after the first dose
2) 2-3 weeks out
3) lasts 1-2 weeks after drug is removed (Craving persists though)

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42
Q

Physical dependence & opioids

1) what is it
2) when does it begin
3) peak
4) length

A
  • onset of withdrawal symptoms once drug is abruptly removed
    2) severe cases, 6-10 hours after last dose
    3) peak 2-3 days after
    4) 5 days for PHYSICAL symptoms (psychological persists)
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43
Q

Symptoms of opioid withdrawal

A
  • body aches
  • diarrhea
  • fever, sweating
  • goose flesh, shivering
  • insomnia, uncontrollable yawning
  • irritability
  • leg cramps/tremors
  • loss of appetite, stomach cramps
  • nausea/vomiting
  • runny nose, sneezing
  • tachycardia
  • weakness/fatigue
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44
Q

What is opioid induced hyperalgesia

A

Fail to respond to opioids or report increased pain when given opioids, even before tolerance develops - not fully understood but probably genetics

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45
Q

Where are the most common drugs involved in prescription opioid overdose deaths

A

Methadone, oxycodone (OxyCotin), hydrocodone (Vicodin)

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46
Q

What is medical assisted treatment (MAT)?

Examples

A
  • use of less addictive/strong opioids to bridge the gap rather than quitting cold turkey
  • buprenorphine: mixed agonist and antagonist
  • methadone (agonist but less side effects)
  • naltrexone (long term IM injections)
47
Q

What do NSAIDs do

A
  • decrease inflammation
  • relieve mild to moderate pain
  • decrease elevated body temp associated with fever
  • decrease blood clotting by inhibiting platelet aggregation
48
Q

What produces the prostaglandin precursor in the body

A

Produced by everything except RBCs and have a normal pathological function

49
Q

What is the biosynthesis of eicosanoids

A

There are two pathways, LOX which yields leukotrienes and COX that yields prostaglandins and thromboxane –> ASA and NSAIDS act on the cox system

50
Q

Why do we care about eicosanoid biosynthesis

A

If cells are subject to trauma, it increases production of prostaglandins, leading to pain, fever, inflammation, dysmenorrhea and thrombus formation

51
Q

What are the two subtypes of COX enzymes and what do they do

A

COX-1: always present and produce prostaglandins for normal cellular activity

COX-2: Produced by injured cells to mediate pain and other aspects of the inflammatory response

52
Q

Basic function of Nonselective NSAID

A

Inhibits both COX-1 and COX-2, decreasing pain/inflam via COX-2 and also dec normal protective prostaglandins causing Stomach and kidney damage

53
Q

Basic function of COX-2 Inhibitor

A

decrease pain and inflammation w/o negative COX-1 gastric and renal side effects

54
Q

What is the dose of OTC vs prescription NSAIDs

A

OTC is 1/3 the dose of prescription

55
Q

What is the OG NSAID

A

Acetylsalicyclic acid (ASA) = Asprin

56
Q

What is the clinical application of aspirin-like drugs

A

Treat mild-moderate pain (OA,RA, dysmenorrhea, minor sx),inflammation and fever (except for those in children), vascular disorders, and prevention of cancer

57
Q

What is Reye syndrome

A

A neurological problem that can occur when aspirin is taken in children

58
Q

ASA influence on vascular disorders

A

It inhibits platelet induced thrombus formation and may prevent the onset or recurrence of MI, TIA and stroke

59
Q

What are the adverse effects of Aspirin-like drugs

A

GI problems (Stomach discomfort, upper GI hemorrhage and ulceration)
CV problems (increased BP to then increase platelet formation)
Inhibit healing of fractures
Hepatotoxicity
Problems with kidney function

60
Q

What are the symptoms of overdose of aspirin and aspirin-like drugs

A 
Tinnitus
Headache
Trouble hearing
Confusion
GI Issues
61
Q

ASA vs other NSAIDs (ie ibuprofen)

A

Same: anti-inflammatory and analgesia
Dif: non-aspirin have less GI effects (still have them) and are less toxic to liver and kidneys

62
Q

What are COX-2 Inhibitors

A

Comparable to nonselective NSAIDs w/lower incidence of GI distress (altho still occurs) and have an increased risk of upper respiratory tract infections, and CV events

63
Q

Do COX-2 drugs increase the risk of MI/CVA? Why or why not?

A

Yes because it decreases the prostaglandins that cause vasodilation and prevent thrombosis, now at an increased risk of developing a clot

64
Q

NSAID pharmacokinetics

A
  • ASA absorbed in stomach and small intestine w/8-90% bound to plasma proteins
  • ASA metabolized in the BLOODSTREAM
  • ASA excreted in the kidneys
65
Q

Acetaminophen vs NSAIDs

A

Same in analgesic and antipyretic (fever) properties HOWEVER acetaminophen does not have the anti-inflammatory or anticoagulant effects
(also acetaminophen can treat fever in children and NSAIDs cannot)

66
Q

What was the first drug used to treat OA

A

Acetaminophen

67
Q

What is the mechanism of action of acetaminophen

A

It is not fully understood how it inhibits the cox enzymes without leading to anti-inflammatory or anticoagulant effects

68
Q

How is acetaminophen metabolized

A

In the liver, it is metabolized to NAPQI which forms with GSH to form mercapturic acid to be eliminated
BUT if NAPQI accumulates it is toxic to the liver and can be fatal

69
Q

What drug is combined with opioid after surgery? Why?

A

Acetaminophen to try and use less opioids to control the pain. Can be taken in combo or w/one extended release opioid w/acetaminophen in b/t to hold over

70
Q

-cet or -tab

A

acetaminophen and opioid combos

71
Q

Acetaminophen pharmacokinetics

A

Absorbed in upper GI tract

  • plasma protein binding is highly variable
  • metabolized in liver
  • excreted inu rine
72
Q

Mm spasms vs spasticity

A

Spasticity is due to CNS injury w/a velocity dependent mm stretech reflex whereas mm spasms are from MSK injury w/involuntary tension of specific mm

73
Q

What is diazepam mechanism for MSK

A

Increases the inhibitory effects of GABA, esp on the alpha motor neuron, to cause generalized sedative effects w/mm relaxation (also used as anti-anxiety agent)

74
Q

T or F: Diazepam produced tolerance and physical dependence

A

True!

75
Q

What are polysynaptic inhibitors

A

may decrease polysnaptic reflex activity in the SC used for ST relief of mm spasms in acute MSK injuries

76
Q

What are the side effects of polysynaptic inhibitors

A

Drowsiness, dizziness, nausea, H/A, vomiting

77
Q

What are 2 examples of polysynaptic inhibitors and how do they work

A
  • Cyclobenzaprine (flexeril): increase seratonin activity in the BS
  • Carisoprodol (soma): may affect GABA-A, producing sedation similar to diazepam
78
Q

What are two types of drugs to treat MSK mm spasms

A

Diazepam

Polysynaptic Inhibitors

79
Q

What is Dantrolene Sodium (Dantrium)

A

A peripherally acting antispasticity agent that inhibits Ca+ release from the sarcoplasmic retic in skeletal mm –> dec. mm contraction and enhanced relaxation

80
Q

What are the side effects of dantrolene sodium

A

mm weakness and hepatotoxicity

81
Q

What is Botox

A

a peripherally acting antispasticity agent that works at the neuromuscular junction to prevent ACh release so the mm can’t contract

82
Q

What is the clinical use of Botox

A
  • treat localized mm dystonia
  • can be injected into bladder detrusor mm to treat neurogenic bladder
  • relief lasts about 3 months
  • reduce spasticity enough so joint and mm can be stretched
83
Q

Limitations and adverse effects of BoTox

A
  • not a cure
  • only lasts up to 3 mo and can only treat 1-2 mm groups at a time
  • CAN SPREAD (low incidence) causing systemic effects like difficulty speaking/swallowing and respiratory disress
84
Q

What is Tizanidine (zanaflex)

A

A centrally acting antispasticity agent primarily used to control spasticity resulting from spinal lesions by binding to alpha-2 adrenergic agonists (dec excitory NT)

85
Q

What is the concern w/tizanidine

A

possibly can slow down neural recovery in acute phase of CVA and TBI`

86
Q

What are the side effects of tizanidine

A

sedation, dizziness, and dry mouth

87
Q

What is Baclofen

A

A centrally acting antispasticity agent that binds preferentially to GABA-B receptors, acting as an agonist to decrease alpha motor neuron activity in the SC

88
Q

What are the side-effects of baclofen

A

drowsiness, fatigue, and mm weakness

89
Q

T or F: Tolerance can occur w/baclofen

A

True - and then when you increase the dose to adjust, it can lead to increased drowsiness

90
Q

What are the indications for intrathecal baclofen

A

severe, intractable spasticity

- long term treatment

91
Q

What is are the positives and negatives of intrathecal baclofen

A
  • allows for increased drug effectiveness w/much smaller drug doses
  • leads to functional movements

negatives: pump malfunction and tolerance

92
Q

What is dizaepam

A

Centrally acting antispaticity agent that works on both skeletal mm spasms and spasticity of CNS origin

93
Q

Pharmacokinetics of mm relaxants

A
  • oral most common route so absorbed by GI
  • metabolized in the liver
  • excreted in the kidneys
94
Q

What are the rehab concerns w/mm relaxants

A
  • Long term use is not practical as it leads to sedation and addictive properties
  • PT can help Pts adjust to sudden changes
95
Q

What are 3 ways to reduce mm excitability

A
  • Act on SC
  • Act at neuromuscular junction
  • act directly w/in skeletal mm fiber
96
Q

What is RA

A

A chronic, systemic autoimmune disorder that is primarily synovitis causing pain, stiffness, and inflammation in smaller –> larger joints

97
Q

T or F: RA is constantly exacerbated

A

FALSE! It has periods of exacerbation and remission that is overall progressive

98
Q

T or F: RA is more common in young men

A

False it is more common in women and older patients

99
Q

What are the 2 goals of drug therapy for RA

A
  1. decrease joint inflammation

2. arrest the progression of the disease

100
Q

What 3 groups of drugs used for RA

A

NSAIDs and glucocorticoids to decrease jt inflammation

DMARDs to slow disease progression

101
Q

What are glucocorticoids

A

Anti-inflammatory agents to decrease joint inflammation and decrease pain and progression of RA BUT there are high adverse effects from high doses of steroids if used alone

102
Q

How are glucocorticoids utilized in treating RA

A

Early on they control pain and inflammation and “bridge” to when DMARDs begin
- then help during exacerbations by increasing dosing at that time

103
Q

Mechanism of Action of Glucocorticoids

A

Bind to specific genes that regulate inflammatory process and inhibit pro-inflammatory substances and increase anti-inflammatory substances

104
Q

What are the adverse effects of glucocorticoids

A
  • catabolic breakdown (mm, bone, ligaments, skin)
  • increased risk of infection
  • increase in mood changes
  • hypertension
  • hyperglycemia
  • increased appetite and weight gain
105
Q

What are the two categories of DMARDs

A

traditional (non-biological) and biological

both control synovitis

106
Q

How are DMARDs used in RA

A

use two or more to attack disease from multiple MoA

107
Q

What is the order of DMARD prescription for RA

A
  1. Methotrexate
  2. TNF-alpha inhibitor
  3. other DMARDs substituted for TNF-alpha
108
Q

Rehab concerns for those w/RA

A

Side effects of gluco (weakness, osteoporosis/osteopenia), side effects of DMARDs (N/H, increased risk of infection)

109
Q

What is osteoarthritis

A

Intrinsic defect in remodeling of the joint cartilage and underlying bone where it is being broken down faster than it can be repaired

110
Q

T or F: Pharmacological management is the first line of defense for OA

A

FALSE - it should be PT, weight loss, and joint replacement in advanced stages

111
Q

What are the two pharmacological treatment goals/categories for OA

A
  • pain relief

- Disease-modifying osteoarthritic drugs (DMOADs)

112
Q

How is analgesia given for OA

A
  • 1st a patch
  • Acetaminophen first
  • NSAIDs better once moderate to severe pain
113
Q

What is viscosupplementation OA

A
  • a DMOD injected into the joint space to replace synovium and liit articular destruction, lasting 6mo –> 1 year
114
Q

What are glucosamine and chondroitin sulfate

A

Nonprescription dietary supplements used to assist w/OA as they are needed for production of cartilage and synovial fluid

UM - Pharmacology (4 decks)

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