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Pharmacology > Pain and Analgesic Drugs (Opioids), NSAIDs, Steroidal Anti-Inflammatory > Flashcards

Pain and Analgesic Drugs (Opioids), NSAIDs, Steroidal Anti-Inflammatory Flashcards

1
Q

What is nociceptive pain? what are examples?

A

Pain that arises from actual or threatened damage to non-neural tissue and is due to
the activation of nociceptors
Post op pain, mechanical LBP, sports injuries, sickle cell crisis, arthritis

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2
Q

what are examples of acute pain?

A

post surgical, headache, trauma

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3
Q

what are examples of central neuropathic pain?

A

post stroke, MS, SCI, phantom pain

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4
Q

what are examples of peripheral neuropathic pain?

A

post- herpetic neuralgia, diabetic neuropathy, HIV related neuropathic pain

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5
Q

Describe pain nerve fibers

A

AB fibers: non noxious mechanical stimulus
AD fibers: noxious mechanical stimulus
C fiber: noxious heat and chemical stimuli

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6
Q

what is the definition of pain?

A

Pain is an unpleasant sensory and emotional
experience associated with actual or potential
tissue damage or described in terms of
such damage

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7
Q

what are possible descriptors of neuropathic pain?

A

numbness, tingling, burning, paresthetic, paroxysmal, electric like, raw, shooting, deep dull

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8
Q

What is allodynia?

A

pain from a stimulus
that does not normally evoke pain (thermal or mechanical)

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9
Q

What is hyperalgesia?

A

exaggerated
response to a painful stimulus

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10
Q

What is neuropathic pain? what are examples?

A

Pain caused by a lesion or damage or disease of the neurons or somatosensory
nervous system.
Post-herpetic neuralgia, neuropathic LBP, distal polyneuropathy, central post stroke pain, trigeminal neuralgia, CRPS

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11
Q

Compare and contrast acute vs chronic pain

A

Acute pain: cause is generally known, duration is short and well recognized, treatment is usually tailored towards resolution of the underlying cause (typically self limiting)
Chronic pain: cause is often unknown, duration is greater than 3 months, treatment is usually geared towards the underlying cause and pain disorder; outcome is often pain control and not cured

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12
Q

what is hyperparethesias?

A

exaggerated
response to touch

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13
Q

what is hyperpathy?

A

persistent pain even after the cause of the pain has been removed

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14
Q

what are some common conditions with neuropathic pain?

A

DM peripheral neuropathy, post herpetic neuralgia, SCI, neuropathic cancer pain, chemotherapy induced neuropathy, CRPS, fibromyalgia, lupus, MS

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15
Q

what is neuralgia vs neuritis?

A

Neuralgia: pain in the distribution of a nerve or nerves
Neuritis: inflammation of a nerve or nerves

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16
Q

List out the treatment options for mild, moderate, and severe pain as per WHO analgesic ladder

A

Step 1 Mild Pain: nonopiod analgesics and NSAIDs + PT OT
Step 2 Moderate Pain:
weak opioids + PT OT
Step 3: Severe Pain:
strong opioids + PT OT
Step 4: Acute, Chronic, Palliative: PT + OT
Adjuvant pain medications at each stage if needed

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17
Q

what are adjuvant drugs?

A

meds not typically for pain but can be helpful for management
antidepressants, antiseizure, muscle relaxant, sedatives, anti anxiety, botulinum toxin

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18
Q

What are the classes of drugs used for the treatment of pain?

A
  1. Nonopioid analgesics are composed of drugs such as
    acetaminophen, aspirin, ibuprofen, and similar agents.
  2. Opioid analgesics are a group of naturally occurring,
    semisynthetic, and synthetic agents that are characterized
    by their ability to relieve moderate-to-severe pain
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19
Q

what are opioid analgesics?

A

Any naturally occurring,
semi-synthetic or synthetic
compound that bind specifically to
opioid receptors and share the
properties of one or more of the
naturally occurring endogenous
opioids.
Narcotics: Morphine, Oxycodone, Fentanyl

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20
Q

what are non-opioid analgesics?

A

NSAIDs
Ibuprofen, Naproxen, Acetaminophen, Celocoxib

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21
Q

What are endogenous opioid peptides and opioid receptors

A

Endogenous opioid peptides: endorphins, enkephalins, dynorphins
Opioid receptors: agonists, antagonists, mixed agonist-antagonist

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22
Q

What are strong agonists? What are they used for?

A

Strong agonists are used to treat severe pain. These drugs have a high affinity for opioid receptors and are believed to interact primarily with mu opioid receptors in the CNS
* Fentanyl
* Morphine (MS Contin)
* Hydromorphone (Dilaudid)
* Oxymorphone (Numorphan)
* Meperidine (Demerol)
* Methadone (Dolophine)
* Oxycodone (Oxycontin)

23
Q

What are mild to moderate agonists? What are they used for?

A

These drugs are still considered agonists that stimulate opioid receptors, but they
do not have as high affinity or efficacy. Used in treating mild to moderate pain.
* Codeine
* Hydrocodone (Hycodan)

24
Q

what are mixed agonist-antagonists?

A

Mixed agonist–antagonist drugs exhibit some agonist and antagonist like activity at the same time because the drugs have the ability to act differently at specific classes of opioid receptors.
* Buprenorphine (Buprenex)
* Nalbuphine (Nubain)

25
Q

what are antagonists? what are they used for?

A

Antagonists block all opioid receptors, with a particular affinity for the mu variety. Because of their antagonistic properties, these agents will not produce analgesia but will displace opioid
agonists from the opioid receptors and block any further effects of the agonist molecules. Antagonists are used primarily to treat opioid overdoses and addiction.
Naloxone, Naltrexone

26
Q

what is the primary agent in the US to treat opioid overdose?

A

The primary agent currently used in the United States to treat opioid overdose is naloxone (narcan).
When administered in emergency situations, this drug can rapidly (within 1 to 2 minutes) and dramatically reverse the respiratory depression that is usually the cause of death in excessive
opioid ingestion.

27
Q

what are primary agents used clinically as opioid antagonists?

A

The primary agents used clinically as opioid antagonists are naloxone (Narcan) and naltrexone (ReVia, Vivitrol)

28
Q

what is the mechanism of action of opioids?

A

Opioid drugs bind to opioid receptors (U,K,D) and will
1. close voltage gated Ca+ channels on presynaptic nerve terminals and reduce release of glutamate and substance p
2. open K+ channels on postsynaptic neurons and hyperpolarize them and inhibit postsynaptic neurons

29
Q

What are key pharmacological actions of opioid agents?

A

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

30
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

31
Q

what are the peripheral effects of opioids?

A

CV system:
*Bradycardia
* Hypotension
* Increase cerebral blood flow (decreased Pco2)
* Increase intracranial pressure
GI system:
* Constipation
Biliary tract:
* Biliary colic
Renal system:
* decreased renal function, urinary retention
Endocrine system:
*decreased testosterone, decreased libido, amenorrhea
Pruritis:
*increased flushing and warmth of the skin

32
Q

what are the clinical uses of opioid analgesics?

A

*Analgesia (Pain relief)
* Acute pulmonary edema
* Cough
* Diarrhea
* Anesthesia

33
Q

What is the opiate toxicity triad?

A

CNS depression (coma), respiratory depression (cyanosis), pupillary miosis

34
Q

What are the adverse affects of opioids with acute use?

A

respiratory depression, nausea, vomiting, constipation, urinary retention, delirium, sedation, myoclonus, seizures

35
Q

what are the adverse effects of chronic opioid use?

A

hypogonadism, immunosuppression, increased feeding, increased GH, withdrawal effects, tolerance, abuse, addiction, hyperalgesia, impairment while driving

36
Q

What pharmacological effects of opioid develop tolerance and what pharmacological effects does not develop tolerance?

A

Tolerance develops to analgesic, sedating, respiratory depressants, the antidiuretic, emetic, and hypotensive effects
* Tolerance does not develop to the miotic, convulsant, and
constipating actions.

37
Q

What is physical dependence and symptoms of withdrawal?

A

Physical Dependence is an invariable accompaniment of tolerance to repeated administration of an opioid of the μ type.
* Symptoms of withdrawal include rhinorrhea, lacrimation, yawning, chills, gooseflesh (piloerection), hyperventilation, hyperthermia, mydriasis,
muscular aches, vomiting, diarrhea, anxiety, and hostility

38
Q

What are special considerations for PT with regard to opioids?

A

Sedation, GI discomfort, respiratory depression, constipation

39
Q

Compare and contrast COX-1 and COX-2

A

COX1: produces PGs that mediate homeostatic functions (gastric protection)
COX2: produces PGs that mediate inflammation, pain, fever and induced mainly in sites of inflammation by cytokines

40
Q

What are Cox-2 selective drugs and what do they do?

A

Celecoxib, Celebrex
Inhibit synthesis of PGs that cause pain, inflammation and spares production of beneficial PGs in stomach, kidney, for normal platelet
function.
* May ↓ pain & inflammation with less toxicity
* Helpful for persons who need to be on NSAIDs long term-OA
* Allow patients to remain active

41
Q

what effect do NSAIDs have on PGs

A

NSAIDs inhibit the synthesis of PGs by inhibiting cyclooxygenase enzymes

42
Q

What are common NSAIDs

A

Aspirin, Ibuprofen, Naproxen, Indomethacin, Meloxicam, Diclofenac, Celecoxib

43
Q

List out therapeutic uses of NSAIDs

A

*Analgesic
*Anti-inflammatory
*Antipyretic
*Anticoagulant
*Anticancer
All above therapeutic effects are thought to be mediated
through inhibition of prostaglandins (PG)

44
Q

what are the effects and indications for acetaminophen?

A

Effects: analgesic and antipyretic effect, no gastric irritation, no anticoagulant effect, no anti-inflammatory effects, possible liver toxicity with high doses
Indications: 1st drug used to control pain in the early stages of OA or other conditions that do not have an inflammatory component

45
Q

what is the MOA of acetaminophen?

A

inhibits the COX enzyme and likely preferentially inhibits CNS PG production

46
Q

Compare and contrast non-steroidal anti-inflammatory drugs and Steroidal Anti-inflammatory drugs

A

Non-steroidal anti-inflammatory drugs: mild to mod inflammation and needs to be taken continuously
Steroidal Anti-inflammatory drugs: powerful anti-inflammatory and immunosuppressive effect, glucocorticoids

47
Q

what are steroidal anti-inflammatory drugs (SAIDs)?

A

the steroids are compounds with glucocorticoid activity and are more powerful than NSAIDs

48
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

49
Q

what is the MOA of glucocorticoids?

A

Act on inflammatory cells (macrophages,
leukocytes). Drug binds to glucocorticoid receptors in
cytoplasm
* Drug-receptor complex travels to nucleus of
the cell and alters gene expression by binding to
glucocorticoid response elements (GREs)
* Decrease expression of inflammatory proteins
(cytokines)
* Increase expression of anti-inflammatory
proteins

50
Q

What is the clinical use of glucocorticoids?

A

Endocrine Conditions: used to normalize adrenal cortical hypofunction (primary
and secondary adrenal insufficiency.)
Nonendocrine Conditions: work on a variety of
conditions for the purpose of either anti-
inflammatory or immunosuppressive effects.
(RA, myositis, tenosynovitis, collagen diseases)

51
Q

what are some glucocorticoid drugs?

A

most will end in -sone
Cortisone
Dexamethasone
Prednisone
Hydrocortisone

52
Q

what are the adverse effects of glucocorticoid drugs?

A

*adrenocortical suppression
*peptic ulcers
*drug induced Cushing syndrome
*adrenal crisis/shock
*breakdown of supporting tissues
*decrease the body’s ability to absorb calcium leading to osteoporosis and delayed wound healing

53
Q

what is the presentation of someone with drug induced Cushing syndrome (hypercortisolism)?

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

54
Q

What are PT considerations for patients taking glucocorticoids?

A

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

Pharmacology (14 decks)

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