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PHTH 561: Pharmacology > Analgesics: Opioids, NSAIDs, & Steroidal Anti-Inflammatories > Flashcards

Analgesics: Opioids, NSAIDs, & Steroidal Anti-Inflammatories Flashcards

1
Q

What is allodynia?

A

Pain due to a stimulus that does not normally provoke pain

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2
Q

What is hyperalgesia?

A

Increased pain from a stimulus that normally provokes pain

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3
Q

What is hypoalgesia?

A

Diminished pain in response to a normally painful stimulus

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4
Q

What is neuralgia?

A

Pain in the distribution of a nerve or nerves

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5
Q

What is neuritis?

A

Inflammation of a nerve or nerves

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6
Q

What is nociception?

A

The neural process of encoding noxious stimuli

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7
Q

What is a nociceptor?

A

A high threshold sensory receptor of the peripheral somatosensory nervous system that is capable of transducing and encoding noxious stimuli

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8
Q

What is nociceptive pain?

A

Pain that arises from actual or threatened damage to non-neural tissue and is due to the activation of nociceptors

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9
Q

What is neuropathic pain?

A

Pain caused by a lesion or damage or disease of the neurons or somatosensory nervous system

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10
Q

What is the WHO analgesic ladder?

A

-Step 1: Mild pain
-Step 2: Moderate pain
-Step 3: Severe pain
-Step 4: Acute, chronic, and palliative

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11
Q

What medications or treatment is used for step 1 on the WHO analgesic ladder?

A

-PT
-OT
-Non-opioid analgesics
-NSAIDs
-Adjuvant pain medications

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12
Q

What medications or treatment is used for step 2 on the WHO analgesic ladder?

A

-PT/OT
-Weak opioids
-Psychology, behavioral therapy, etc.

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13
Q

What medications or treatment is used for step 3 on the WHO analgesic ladder?

A

-Strong opioids
-PT/OT
-Psychology, behavioral therapy, etc.

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14
Q

What medications or treatment is used for step 4 on the WHO analgesic ladder?

A

-PT
-OT

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15
Q

What treatments can be used at every step on the WHO analgesic ladder?

A

-NSAIDs
-PT/OT
-Acupuncture
-Massage
-TENS

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16
Q

What is adjuvant pain medications?

A

Medications that are not typically used for pain but may be helpful for its management

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17
Q

What are some examples of adjuvant pain medications?

A

-Anti-depressants
-Anti-seizure medications
-Muscle relaxants
-Sedatives
-Anti-anxiety medications
-Botulinum toxin

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18
Q

What are medications that help to alter the perception of pain in the brain?

A

-Opioids
-TCAs
-SSRI
-SNRIs
-⍺-2 agonists

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19
Q

What are medications that help to modulate the ascending/descending pain pathway?

A

-TCAs
-SSRIs
-SNRIs

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20
Q

What are medications that limit the transmission of pain in the peripheral nerves?

A

-LAs (ask Dr. Pattipatti what this is)
-Opioids
-⍺-2 agonists

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21
Q

What are medications that limit the transduction of peripheral nociceptors?

A

-LAs
-Capsaicin
-Anticonvulsants
-NSAIDs
-ASA (what is this?)
-Acetaminophen
-Nitrate

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22
Q

What are examples of TCAs and SSRIs?

A

-Amitriptyline
-Noritryptiline
-Duloxetine

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23
Q

What are examples of topical agents?

A

-Capsaicin
-Lidocaine patch

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24
Q

What are examples of opioids?

A

-Tramadol
-Tapentadol
-Hydrocodone
-Oxycodone
-Methadone

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25
Q

What are examples of NMDA inhibitors?

A

-Ketamine
-Amantidine
-Memantine

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26
Q

What are examples of anticonvulsant agents?

A

-Pregabalin
-Gabapentin
-Carbamazepine

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27
Q

Where does opioids come from? What is the history of its use?

A

-Exudate from the opium poppy
-Has been used for 2,000-6,000 years
-Known to relieve pain, diarrhea, and produce euphoria
-Serturner isolated and puriphied morphine in 1803
-Semisynthetic compounds (Heroin- 1874)
-Fully synthetic opioids (Meperidine- 1939)
-Medicinal and recreational uses firmly established

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28
Q

Where are endogenous opioids derived from?

A

Peptides

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29
Q

Where are endorphins derived from? What types of endorphins are there? What receptors do they work on?

A

-Derived from proopiomelanocortin (POMC)
-2 types of β-endorphins: β-endorphin-1 and β-endorphin-2
-Primarily µ agonist and also has 𝛿 action

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30
Q

Where are enkephalins derived from? What types are there? What receptors do they work on?

A

-Derived from proenkephalin
-Met-ENK
-Leu-ENK
-Met-ENK: µ and 𝛿 agonist
-Leu-ENK: 𝛿 agonist

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31
Q

Where are dynorphins derived from? What types are there? What receptors do they work on?

A

-Derived from prodynorphine
-DYN-A
-DYN-B
-Potent 𝜿 agonist and also have µ and 𝛿 action

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32
Q

What are the 3 opioid receptors? What therapeutic effects does agonists of these receptors create?

A

-Mu (µ)
-Kappa (𝜿)
-Delta (𝛿)
-Creates spinal and supraspinal analgesia

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33
Q

What are other effects of µ agonists?

A

-Sedation
-Respiratory depression this is why opioid overdose can cause death
-Constipation
-Inhibits neurotransmitter release (ACh, dopamine)
-Increases hormonal release (prolactin, growth hormone)

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34
Q

What are other effects of 𝜿 agonists?

A

-Sedation
-Constipation
-Psychotic effects

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35
Q

What are other effects of 𝛿 agonists?

A

-Increases hormonal release (growth hormone)
-Inhibits neurotransmitter release (dopamine)

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36
Q

What are opioid receptor agonists?

A

Activate one or more opioid receptors

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37
Q

What are opioid receptor antagonists?

A

Occupy receptors and prevent agonist binding (e.g. Naloxone)

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38
Q

What are opioid mixed receptor agonist-antagonists?

A

Agonist activity at one type of receptor and antagonist activity at another type of receptor (e.g. Buprenorphine)

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39
Q

What is the difference between and opioid and an opiate?

A

-Opioid: any naturally occurring, semi-synthetic, or fully synthetic compound that binds to opioid receptors and share the properties of one or more of the naturally occurring endogenous opioids
-Opiate: any naturally occurring opioid derived from opium

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40
Q

What are examples of strong opioid receptor agonists? What receptor do they primarily interact with?

A

-Strong agonists are used to treat severe pain
-Interact primarily with µ receptors
-Fetanyl (Duragesic, Sublimaze)
-Morphine (MS Contin)
-Hydromorphone (Dilaudid)
-Oxymorphone (Numorphan)
-Meperidine (Demerol)
-Methadone (Dolophine)
-Oxycodone (Oxycontin)

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41
Q

What are examples of mild to moderate opioid receptor agonists?

A

-These are used for mild to moderate pain
-Codein
-Hydrocodone (Hycodan)

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42
Q

What are examples of mixed opioid receptor agonist-antagonist?

A

-Some of these bind to 𝜿 receptors while block or partially block µ receptors making them µ receptor antagonists or partial agonists
-Buprenorphine (Buprenex)
-Nalbuphine (Nubain)

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43
Q

What are examples of opioid receptor antagonists?

A

-Particular affinity for µ
-Naloxone (Narcan)
-Naltrexone (ReVia, Vivitrol)

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44
Q

What are other uses of Naltrexone?

A

-Can be used in conjunction with behavioral therapy to maintain an opioid-free state for recovering opioid addicts
-Can be used in treating alcohol dependence

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45
Q

What is the mechanism of action of opioids?

A

-Bind to opioid receptors
-Two well established direct G-protein coupled actions
-They close voltage gated Ca2+ channels on presynaptic nerve terminals which reduces neurotransmitter release (glutamate and substance P)
-They open K+ channels on postsynaptic neurons and hyperpolarize them and inhibit postsynaptic neurons

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46
Q

What are the sites of putative action of opioid analgesics?

A

-Primary afferent nociceptor terminals
-Dorsal horn
-Ventral posterolateral nucleus (VPL) of the thalamus
-Possibly in the amygdala as well

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47
Q

What are the key pharmacological actions of morphine and other opioid agents?

A

-Analgesia
-Respiratory depression
-Spasm of smooth muscle of the gastrointestinal (GI) and genitourinary (GU) tracts, including the biliary tract (bile ducts)
-Pinpoint pupils (miosis)

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48
Q

What is a way to determine if someone if overdosing from opioids or another drug?

A

If someone’s pupils are constricted/has pinpoint pupils, they are overdosing from opioids

49
Q

What are the CNS effects of opioids?

A

-Analgesia
-Euphoria
-Sedation
-Respiratory depression
-Cough suppression
-Miosis
-Truncal rigidity
-Nausea and vomiting
-Body temperature
-Sleep disturbances

50
Q

What are the effects of opioids on the cardiovascular system?

A

-Typically no significant effects
If there are effects:
-Bradycardia
-Hypotension
-Increased cerebral blood flow
-Increased intracranial pressure (opioids contraindicated in brain injury patients)

51
Q

What are the effects of opioids on the gastrointestinal system?

A

Constipation

52
Q

What are the effects of opioids on the biliary tract?

A

Biliary colic (blockage of bile ducts- contraction of biliary smooth muscles)

53
Q

What are the effects of opioids on the renal system?

A

-Decreased renal function
-Anti-diuretic effect
-Urinary retention

54
Q

What are the effects of opioids on the endocrine system?

A

-Decreased testosterone with chronic use
-Decreased libido, energy, and mood
-Dysmenorrhea or amenorrhea in women

55
Q

What are the effects of opioids on the skin?

A

-Pruritis (itchy feeling of the skin)
-Produce flushing and warming of the skin accompanied sometimes by sweating, urticaria (itchy red bumps), and itching
-Peripheral histamine release

56
Q

What is the duration of action of fentanyl?

A

1 hour

57
Q

What is the duration of action of methadone?

A

8 hours

58
Q

What is the duration of action of morphine?

A

4 hours

59
Q

What is the duration of action of oxycodone?

A

4 hours

60
Q

What is the duration of action of codeine?

A

4 hours

61
Q

What is the duration of action of hydrocodone?

A

4 hours

62
Q

What is the duration of action of tramadol?

A

4 hours

63
Q

What is the duration of action of buprenorphine?

A

5 hours

64
Q

What is the duration of action of naloxone?

A

2 hours

65
Q

What is the duration of action of naltrexone?

A

24 hours

66
Q

What are the clinical used for opioids?

A

-Analgesia
-Acute pulmonary edema
-Cough
-Diarrhea
-Anesthesia

67
Q

What are the signs & symptoms of opioid overdose?

A

-Euphoria
-Unconsciousness
-Respiratory depression
-Miosis
-Pulmonary edema
-Seizures
-Hypothermia
-Death

68
Q

What is the opiate toxicity triad?

A

-CNS depression (coma)
-Respiratory depression (cyanosis)
-Pupillary miosis

69
Q

What are adverse effects with chronic opioid use?

A

-Hypogonadism
-Immunosuppression
-Increased feeding
-Increased growth hormone secretion
-Withdrawal effects
-Tolerance, dependence
-Abuse, addiction
-Hyperalgesia
-Impairment while driving

70
Q

What does a person develop tolerance for on opioids?

A

-Analgesic effect
-Sedating effect
-Respiratory depressant effects
-Antidiuretic, emetic, and hypotensive effects

71
Q

What tolerance does not develop on opioids?

A

-Mitotic effect
-Convulsant effect
-Constipating effect

72
Q

What is physical dependence of opioid use?

A

An invariable accompaniment of tolerance to repeated administration pf an opioid of the µ type

73
Q

What are symptoms of withdrawal to opioids?

A

-Rhinorrhea
-Lacrimation
-Yawning
-Chills
-Gooseflesh
-Hyperventilation
-Hyperthermia
-Mydriasis
-Muscular aches
-Vomiting
-Diarrhea
-Anxiety
-Hostility

74
Q

What is psychological dependence of opioids or other drugs?

A

Addiction

75
Q

What are benefits of patient controlled anesthesia?

A

-May allow better pain control with fewer side effects
-Requires patient awareness and cognitive ability
-Increases patient satisfaction

76
Q

What are special concerns for rehab with opioids?

A

-Schedule therapy when drugs reach peak
-Consider respiratory depression
-Constipation: pts may be uncomfortable
-Withdrawal symptoms or addiction

77
Q

What are non-opioid analgesics?

A

-Non-steroidal anti-inflammatory drugs (NSAIDs)
-Acetaminophen (Tylenol)

78
Q

What are the primary therapeutic effects of NSAIDs?

A

-Analgesic
-Anti-inflammatory
-Antipyretic (reduces body temp.)
-Anticoagulant
-Anticancer (colorectal cancer)

79
Q

What are prostaglandins (PGs)?

A

-Small lipid compounds produced in almost all cells
-Cells begin to synthesize PGs in response to damage

80
Q

What are the function of PGs?

A

-In the hypothalamus: thermoregulation
-Responsible for coagulation
-PGs can exaggerate pain
-Promote inflammation
-Abnormal coagulation

81
Q

How are PGs synthesized?

A

Prostaglandings are made by an enzymatic reaction where cyclooxygenase (COX-1, COX-2) converts arachidonic acid into prostaglandins

82
Q

What is the mechanism of action of NSAIDs?

A

NSAIDs inhibit cyclooxygenase (COX-1, COX-2) from converting arachidonic acid to prostaglandins

83
Q

What are non-selective NSAIDs? What are examples of them?

A

-Inhibit COX-1 and COX-2
-Diclofenac
-Ibuprofen
-Naproxen

84
Q

What are COX-2 selective NSAIDs? What are examples of them?

A

-Specifically inhibit COX-2
-Celecoxib (Celebrex)
-Rofecoxib

85
Q

Why if Rofecoxib banned?

A

Due to cardiovascular side effects

86
Q

What are the functions of the prostaglandins that COX-1 produces?

A

-PGs that mediate homeostatic functions
-Constitutively expressed
-Homeostatic protection of gastric mucosa
-Platelet activation
-Renal functions
-Macrophage differentiation

87
Q

What are the functions of the prostaglandins that COX-2 produces?

A

-PGs that mediate inflammation, pain, and fever
-Induced mainly in sites of acute inflammation by cytokines
-Pathologic inflammation
-Pain
-Fever
-Dysregulated proliferation

88
Q

What are common NSAIDs?

A

-Aspirin
-Ibuprofen
-Naproxen
-Indomethacin
-Meloxicam
-Diclofenac
-Celecoxib

89
Q

What are common side effects of NSAIDs?

A

-Nausea and vomiting
-Diarrhea
-Constipation
-Decreased appetite
-Rash
-Dizziness
-Headache
-Drowsiness

90
Q

What are side effects associated with chronic use of NSAIDs?

A

-Kidney failure
-Liver failure
-Ulcers

91
Q

What are uncommon side effects of NSAIDs?

A

-Prolonged bleeding after injury or surgery
-Fluid retention/edema

92
Q

What is the benefit of selective COX-2 NSAIDs vs non-selective NSAIDs?

A

-May decrease pain & inflammation with less toxicity (less gastritis)
-Better for long term use

93
Q

What are the benefits of acetaminophen?

A

-Analgesic and antipyretic effects
-No gastric irritation
-No anticoagulant effects
-No anti-inflammatory effects

94
Q

What are side effects of acetaminophen if taken in high doses?

A

Liver toxicity

95
Q

What are indications for acetaminophen?

A

-Frequently 1st drug used to control pain in early stages of OA and other MSK conditions that do not have an inflammatory
-Children and teenagers

96
Q

What is a contraindication for acetaminophen?

A

-Reyes syndrome
-This syndrome is a rare but serious condition that causes confusion, swelling in the brain, and liver damage

97
Q

What is the mechanism of action of acetaminophen?

A

-Not fully understood
-Inhibits cyclooxygenase (COX)
-Unclear why it does not exert anticoagulant & anti-inflammatory effects: thought to preferentially inhibit CNS PG production vs peripheral

98
Q

Why can high doses of acetaminophen cause liver toxicity?

A

-Acetaminophen metabolizes into a toxic intermediate
-It is quickly detoxified and eliminated via the urine
-High doses can result in accumulation of the toxic intermediate with subsequent toxicity to liver proteins

99
Q

What are common acetaminophen + opioid combinations?

A

-Lortab, Lorcet: hydrocodone + acetaminophen
-Darvocet: propoxyphene + acetaminophen
-Percocet: oxycodone + acetaminophen

100
Q

What are physical therapy considerations for patients on NSAIDs or acetaminophen?

A

-Pain masking
-GI effects
-Cardiovascular risks
-Renal effects
-Hepatotoxicity
-Therapy timing
-Patient education
-Monitoring side effects

101
Q

What are steroidal anti-inflammatory drugs (SAIDs)?

A

-Glucocorticoids
-Derived from cholesterol

102
Q

What three 1° adrenal steroids does the adrenal cortex produce?

A

-Glucocorticoids (cortisol, corticosterone)
-Mineralocorticoids (aldosterone)
-Sex hormones

103
Q

What are the physiological functions of glucocorticoids?

A

-Control glucose metabolism
-Controls the body’s ability to deal with stress
-Decrease inflammation
-Suppress the immune system

104
Q

What is the precursor to steroids?

A

Cholesterol

105
Q

What is the mechanism of action of glucocorticoids?

A

-Act on inflammatory cells
-Drug binds to glucocorticoid receptors in cytoplasm
-Drug-receptor complex travels to nucleus of the cell and alters gene expression
-Decreases expression of inflammatory proteins
-Increases expression of anti-inflammatory proteins

106
Q

What is the clinical use of glucocorticoids?

A

-Endocrine conditions: normalize adrenal cortical hypofunction
-Nonendocrine conditions: RA, tenosynovitis, myositis, collagen disease

107
Q

How are glucocorticoids for nonendocrine conditions such as RA or tenosynovitis administered?

A

Injections into specific tissues to help localize effects

108
Q

What are some common glucocorticoids?

A

-Cortisone
-Dexamethasone
-Prednisone
-Hydrocortisone

109
Q

What glucocorticoid is typically used for anaphylaxis?

A

Dexamethasone

110
Q

What are methods of administering glucocorticoids?

A

-Oral: systemic
-Injections: local
-Dose packs: provide large dose but tapers off over 4-5 day period

111
Q

What are adverse effects of glucocorticoids?

A

-Adrenocortical suppression
-Peptic ulcers
-Drug induced Cushing Syndrome
-Adrenal crisis/shock
-Breakdown of supporting tissues
-Decreases body’s ability to absorb calcium and can lead to osteoporosis

112
Q

What are side effects of glucocorticoids?

A

-Headache
-Irregular heartbeat
-Sweating
-Dizziness
-Irritability

113
Q

How does breakdown of supporting tissues occur from glucocorticoid use?

A

-Bone, ligaments, tendons, and skin are subject to a wasting effect from prolonged use
-Inhibits the genes responsible for production of collagen and other tissue components by increasing the expression of substances that promote breakdown of bone, muscle, etc.
-Interferes with muscle protein synthesis
-Can cause skeletal muscle atrophy

114
Q

What are the signs & symptoms of drug induced Cushing Syndrome?

A

-Roundness and puffiness in the face
-Fat deposition and obesity in the trunk
-Muscle wasting in extremities
-Hypertension
-Osteoporosis
-Increased body hair
-Glucose intolerance

115
Q

What are signs & symptoms of adrenal crisis/shock?

A

-Vasodilation of the organs
-Vascular collapse
-Severe hypotension
-Pain in legs, low back, abdomen
-Low BP, syncope
-Vomiting and diarrhea
-Hyperkalemia
-Hyponatremia

116
Q

How can glucocorticoids lead to osteoporosis?

A

-Shifts the balance of bone metabolism leading to increased breakdown
-Stimulates osteoclast-induced bone resorption
-Inhibits osteoblast-induced bone formation

117
Q

What are other side effects of glucocorticoids?

A

-Salt/water retention
-Increased infection
-Gastric ulcers due to decreased good PGs in stomach
-Glucose intolerance
-Glaucoma-effect vitreous humor drainage
-Adrenal suppression

118
Q

What are PT considerations for glucocorticoid use?

A

-Increased risk of fractures, falls, and infection
-Strengthening exercises to maintain muscle mass
-Encourage weight bearing activities such as walking
-Inspection for skin breakdown
-Monitor blood pressure

PHTH 561: Pharmacology (7 decks)

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