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PHAR 255 Exam 2 > PAIN > Flashcards

PAIN Flashcards

1
Q

Define pain

A

an unpleasant sensory and emotional experience associated with, or resembling that associated with, actual or potential tissue damage

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2
Q

What is critical to understand in a patient experiencing pain?

A

A reported pain experience must be respected

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3
Q

Describe the biopsychosocial model of pain

A

Pain affects all aspects of one’s life
Reduced quality of life and general health
Mental and emotional health
Increased risk of suicide
Problems with cognitive function, such as reduced processing speed, selective attention, memory, and executive functioning
School/work absence and reduced productivity
Increased disability and inactivity
Decreased social connections and supports
Increased health care utilization

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4
Q

What are the classifications of pain?

A
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5
Q

Describe the differences in acute pain and chronic pain?
a) Duration
b) Organic Cause
c) Relief of Pain
d) Tx Goal
e) Dependance/Tolerance to Meds
f) Psychological Component of Pain
e) Environmental/familty issues
f) Depression
g) Insomnia

A
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6
Q

Define Nociceptive Pain?

A

Arises from damage to body tissue; typical pain one experiences as a result of injury, disease, or inflammation

Usually described as sharp, aching, or throbbing pain

e.g., burning your hand on a hot stovetop (tissue damage = adaptive)

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7
Q

Define neuropathic pain

A

Arises from direct damage to the nervous system itself, usually peripheral nerves but can also originate in central nervous system

Usually described as burning or shooting/radiating, the skin might be numb, tingling, or extremely sensitive – even to light touch (allodynia)

e.g., post-herpetic neuralgia (i.e. shingles pain)

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8
Q

Define nociplastic pain

A

Arises from a change in the way sensory neurons function, rather than from direct damage to the nervous system; sensory neurons become more responsive (sensitization)

Usually described similar in nature to neuropathic pain

e.g., fibromyalgia (no tissue damage = maladaptive)

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9
Q

NiciceptivePain: Describe the difference between somatic and viscerail pain

A
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10
Q

Describe the nocicpetive pain pathophysiology

A
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11
Q

Describe nocicpetive pain transduction

A
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12
Q

Describe nocicpetive pain conduction

A
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13
Q

Describe nocicpetive pain transmission

A

A-δand C-nerve fibers synapse in various layers (laminae) of the spinal cord’s dorsal horn
Release excitatory neurotransmitters (e.g. glutamate, substance P)

N-type voltage-gated calcium channels regulate the release of these excitatory neurotransmitters

Pain signals reach brain through various ascending spinal cord pathways (including spinothalamic tract)

Thalamus acts as relay station within brain

Pathways ascend and pass impulses to higher cortical structures for further pain processing

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14
Q

Describe nociceptive pain perception.How does this occur?

A

Pain becomes a conscious experience

Occurs in higher cortical structures

Physiology of perception is not well understood

Cognitive and behavioural functions can modify pain
Relaxation, distraction, meditation may ↓ pain
Depression, anxiety ↑ pain

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15
Q

Describe nociceptive pain modulation

A
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16
Q

Howis neuropathic pain different from nocipetive pain?

A

Different from nociceptive pain
No noxious stimuli
Result of damage or abnormal functioning of the PNS +/- CNS

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17
Q

Difference between peripheral and central neuropathic pain

A
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18
Q

Describe the pathophysiology of nociplastic pain

A
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19
Q

Acute Pain Duration and Cause

A

Typically < 3-6 months

Due to tissue damage signaling harm or potential for harm

Serves a useful purpose (adaptive)

Often due to an identifiable cause
Common causes: surgery, acute illness, trauma, labour, medical procedures

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20
Q

What typoes of pain are acute pain? Issue with long-term pain?

A

Usually nociceptive, sometimes neuropathic

May outlive its biologic usefulness and have negative effects

Poorly treated, can increase risk of chronic pain syndromes, including nociplastic pain (maladaptive)

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21
Q

General Presentation of acute pain

A
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22
Q

Sx of Acute Pain

A
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23
Q

Signs of acute pain

A
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24
Q

Lab Tests and Diagnosis of Acute Pain

A
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25
Q

How can acute pain be assesed?

A

Pain management is most effective when validated and accurate pain assessments are carried out

Self-rated pain intensity scales
Adult: visual analogue or numerical rating scale
Child: Faces scale (Bieri or Wong-Baker)

Observational tools
If unable to communicate
PAINAD (dementia), FLACC (>2 months), CHEOPS (>1yr), PACSLAC (dementia)

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26
Q

Red flags for referral of back pain

A
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27
Q

Algorithm for Pain Assesment

A
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28
Q

Acute Pain Goals of TX

A

Primary goal depends on type of pain present and should be tailored to individual patient and circumstance

Acute pain: achieve level of pain relief that allows patient to attain certain functional goals (usually = get back to normal function) → cure

Realistic pain reduction = may be possible to fully eliminate pain, unlike in chronic pain

Prevent or minimize ADEs
Improve quality of life

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29
Q

Non-Pharm Strategies Acute Pain

A

There is a difference between active and passive strategies – (active – movement, relaxation) – EMPHASIZE active strategies, tend to work the best

Passive strategies should not be used alone (someone doing something to you – acupuncture, meds are passive strategies, massage) – Needs to be combined with active

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30
Q

Pharm Tx Overview of Acute Pain

A
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31
Q

Acet Moa

A

Believed to inhibit prostaglandins in the CNS and work peripherally to block pain impulse generations
Minimal effect on peripheral prostaglandin synthesis (no anti-inflammatory activity)

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32
Q

Acet Place in TX

A

Reduction of fever (1st line)
Mild-moderate acute pain
Pediatric moderate pain
Dementia (more aggressive, self it changes anything for them)

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33
Q

Acet A/e

A

Liver toxicity
Overdose
May increase systolic BP (~3-4mmHg)
Rare neutropenia and thrombocytopenia

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34
Q

Acet C.I

A

Acetaminophen-induced liver disease
Hypersensitivity to acetaminophen, or any component of the formulation

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35
Q

Acet Cautions

A

Acetaminophen is one of the most frequent causes of accidental poisoning in infants and toddlers

Hepatotoxicity has occurred in patients receiving high or excessive doses with therapeutic intent

Some patients may be more susceptible to acetaminophen hepatotoxicity (e.g., chronic alcohol use, those with liver disease, or those who are malnourished or taking other hepatotoxic drugs)

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36
Q

Acet Dosing of AVilable Formulations

A
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37
Q

NSAID MOA

A

Non-Selective:
Inhibit cyclooxygenase-1 and 2 (COX-1 and 2) enzymes, which results in ↓ formation of prostaglandin precursors
Antipyretic, analgesic, and anti-inflammatory properties

COX-2 Inhibitors (Coxibs):
Inhibit prostaglandin synthesis by ↓ the activity of the enzyme, COX-2, which results in ↓ formation of prostaglandin precursors
Antipyretic, analgesic, and anti-inflammatory properties.
Do not inhibit COX-1 at therapeutic concentrations

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38
Q

NSAID Place in TX

A

Mild to moderate pain (osteoarthritis, acute & chronic low back pain)
Dysmenorrhea-induced pain
Fever (only ibuprofen and naproxen)

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39
Q

C.I. NSaids

A

CKD (CrCl < 40mL/min)
Hyperkalemia
Cirrhosis/ Liver impairment
GI Ulcer (duodenal/ peptic) + IBD
Uncontrolled Heart Failure
MI
Thrombocytopenia
Transplant

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40
Q

A/E NSAIDs

A

Dyspepsia
Edema
GI Bleed
N/V
Phototoxic Reaction
CNS : Dizziness, drowsiness, headache, tinnitus, confusion (especially in the elderly & with indomethacin). CNS effects may be dose related.
Minor or serious skin rashes, pruritus
COX-2 selective – similar efficacy & renal/CV toxicity to other NSAIDS, but less GI risk

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41
Q

NSAID CAutions

A

Asthma
CVD, HTN
Risk of bleeding increases perioperatively; discontinue pre-surg

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42
Q

ASA MOA

A

Irreversibly inhibits COX-1 and COX-2 enzymes via acetylation which decreases formation of prostaglandin precursors
Antipyretic, analgesic, and anti-inflammatory properties

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43
Q

Place in TX ASA

A

Mild-moderate pain (short term use)
Reduction of fever

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44
Q

ASA Dosing

A

< 300mg/d: reduce platelet aggregation
300-2400mg/d: antipyretic and analgesic (325-650mg po q4h prn)
2400-4000mg/d: anti-inflammatory
Max: 4g/day

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45
Q

C.I. ASA

A

Hypersensitivity to NSAIDs, anaphylaxis
CKD (CrCl < 40mL/min)
GI Ulcer

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46
Q

A/E ASA

A

Same as NSAIDS

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47
Q

Cautions of ASA

A

Concurrent antiplatelet and/or anticoagulant therapy
Risk of Reye syndrome in children
Toxic in overdose (tinnitus, vertigo, hyperventilation, respiratory alkalosis, hyperthermia, coma, death)

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48
Q

Describe Peripheral PG Synthesis

A
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49
Q

ASA Dose

A

325-650 mg PO q4-6h (PRN)
Max: 4000 mg/day

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50
Q

Diclofenac DOse

A

50 mg PO BID; 75- 100 mg SR PO daily (PRN)
Max: 100 mg/day (Dose-relaed)

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51
Q

Ibuprofen Dose

A

TC: 200-400 mg PO q4-6h (PRN) (max 1200 mg/day)
Rx: 600 mg PO q6h (PRN) (max 2400-3200 mg/day)

Children up to 12 years of age: 4-10 mg/kg/dose q6-8h; max = 40mg/kg/day

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52
Q

Ketorlac Dose

A

10 mg PO QID (PRN)
Max: 40 mg/d, 5 days limit (↑ GI bleed risk)

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53
Q

Naproxen Sodium ()OTC)

A

125 – 500 mg PO BID (PRN)
Max: 1500 mg/day

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54
Q

NAproxen Base Dose

A

250-500 mg PO BID (PRN)
Max: 1000 mg/day

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55
Q

Cardiac Risk of NSaids.. ASA?

A

Thromboxane A2 produced by the COX-1 pathway on activated platelets is platelet aggregating and vasoconstricting

Prostacyclin produced by the COX-2 pathway in nearby smooth muscle cells is a platelet inhibitor and vasodilating

ASA, as a non-reversible COX inhibitor (COX-1 > COX-2), inhibits platelet aggregation even at low doses and is cardioprotective

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56
Q

Cox-2 Inhibitors and Cardiac Risk

A

Selective COX-2 inhibitor NSAIDs “tip the balance” in favour of:
vasoconstriction
platelet aggregation
thrombosis

Other non-selective NSAIDs have varying cardiac risk depending on specificity for COX-1 and COX-2

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57
Q

ASA and NSAID Interaction and MAnagement

A

ASA, Aspirin, Naproxen D.I.

Ibubrofen and naproxen have higher affinity for Cox enzymes (take this before or at same time with ASA) – Ibu and naproxen will bind to platlets reversibley (will lose effect)

Sperate them out
Give advil, wait 2 hours and then give ASA – ASA can get on the platelets and inhibit them

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58
Q

Cardiac vRisk of Avilable NSAID’s and MAngement

A
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59
Q

Which NSAID is the most cardiac neutral

A

Naproxen

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60
Q

How do NSAID’s excaerbate HF and increase blood pressure?

A
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61
Q

How do NSAID’s pose a GI Risk?

A

Prostaglandins produced by the COX-1 pathway increase GI mucosal blood flow, mucous and bicarbonate production, and epithelial growth

NSAIDS inhibit COX-1 which leads to
↓ prostaglandins
↓ gastroduodenal mucosal protection
↑ GI ulcer risk

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62
Q

Management of GI Risk of NSAIDs

A

Consider misoprostol or PPI (add-on or combo product):

Arthrotec 75 (50/75mg diclofenac + 200 mcg misoprostol), generic
Formulary
Max diclofenac is 100 mg a day; may need to adjust dose

Vimovo (375/500 mg naproxen + 20 mg esomeprazole)
Non-formulary

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63
Q

Risk Classification of GI Toxicity of NSAID’s

A
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64
Q

Recommendations for prevention of NSAID complications

A
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65
Q

Renal Risk: How do NSAIDS cause it?

A

Prostaglandins (PGE2, PGI2) produced by the COX-1 and COX-2 pathways are vasodilating
NSAIDs inhibit COX-1 and COX-2 which leads to
vasoconstriction of afferent renal arteriole
↓ ability for kidneys to regulate blood flow

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66
Q

Risk Factors for Renal Dysfx NSAIDs

A

Age ≥70
Pre-existing renal disease
Volume depletion (diuretics)
Combined use with ACEI or ARB (dilate efferent arteriole)
Heart failure
Cirrhosis
Long-term history of NSAID use

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67
Q

Managemnet of Renal Risk NSAIDs

A

Avoid in CKD (CrCl < 40 mL/min)
Monitor creatinine, urea within 3-7 days after initiating therapy

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68
Q

Celecoxib Advantages

A

Main attractive feature is the selective COX-2 inhibition
COX-1 primarily involved in homeostatic bodily functions
Maintains normal lining of the GI tract
Maintains blood patency (hemostasis)

COX-2 primarily involved with pain and inflammation

Selective COX-2 inhibition spares the inhibition of COX-1
↓ the risk of GI complications (e.g., GI bleeding)
minimal platelet effect
↑ cardiac/serious events with celecoxib > 200mg/day

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69
Q

Celecoxib DoseAdjustments and Renal Risk

A

Dose adjustments recommended for elderly and CYP2C9 metabolizers
CYP2C9 poor metabolizers, reduce initial dose by 50%

Carries similar renal risk as non-selective NSAIDs

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70
Q

Celecoxib Dosing

A

Acute pain:
Celecoxib 400mg PO as a single dose on the first day, followed by 200mg PO once daily (up to 7 days); max dose = 400mg/day for up to 7 days

Other indications:
Dose ranges from 100-200mg PO once daily to twice daily (max dose = 200 or 400mg per day, depending on indication)

Dose-related ↑ in serious CV events (e.g., MI) detectable at doses of celecoxib 200mg BID (400mg/d) or more

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71
Q

NSAID/COXIBS D.I.

A

↓ anti-HTN effect: ACE-I, ARB, beta-blocker, thiazides
↑ toxicity of: lithium, methotrexate, steroids, tenofovir, warfarin
↑ risk of GI bleed: warfarin, heparin, corticosteroids, SSRI
↑ nephrotoxicity: ACE-I, ARB, diuretics
↓ efficacy of ASA antiplatelet effect if co-administered

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72
Q

Preganancy and NSAIDs

A

Pregnancy: do not recommend in general
Preconception: query block implantation
1st trimester: malformations, miscarriage
2nd trimester: low dose PRN
3rd trimester: closes ductus arteriosus

Low dose ASA has some pregnancy-related indications (generally avoid higher pain doses)
Should be discussed with obstetrician and/or primary care provider
Low dose for prevention of pre-eclampsia, thromboprophylaxis for positive antiphospholipid antibody test or with confirmed antiphospholipid syndrome

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73
Q

Lactation and NSAID’s

A

Lactation: may consider agents with short half life (can get into the breast milk)
Ibuprofen, diclofenac

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74
Q

Muscle Relaxantas Examples and MOA

A

Centrally-acting drugs via heterogeneous mechanisms

Methocarbamol (sedative  skeletal muscle relaxation)

Baclofen (centrally acting in spinal cord  relief of spasticity)

Cyclobenzaprine (similar to TCA in structure and adverse effects  drug interactions)- ANTICHOLINERGIC

Tizanidine (alpha2-adrenergic agonist (like clonidine)  hypotension)

Little/no actual relaxant effect on tissues  ?misnomer

Effect linked to sedation and resultant central relaxation?

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75
Q

Muscle Relxants Place in TXand Duration

A

Might consider for spasms (acute low back pain)
No evidence that they are more effective than acetaminophen/NSAIDs
Limit use to < 1-2 weeks

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76
Q

C.I. Muscle Relxants

A

Age > 65 years old (although commonly seen in practice)

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77
Q

Cautions of Muscle Relxants

A

++ CNS adverse effects (drowsiness, impaired cognition, falls)
Hepatic toxicity (esp. with Tylenol)
Hypotension (tizanidine)
Risk usually > benefit, esp. in chronic treatment

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78
Q

Dose Muscle RElxants

A

Baclofen 5-20 mg TID
Cyclobenzaprine 5-10 mg TID
Methocarbamol (combo with ASA/acetaminophen/ibuprofen)

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79
Q

Step-wise APproach WHO LAdder

A
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80
Q

Analgesic LAdder RXFiles

A
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81
Q

Pain In specific Populations:
a) Acute on Chronic
b) Incident
c) Frail Elderly
d) Hepatic Dysfx
5. Renal Dysfx
6. Prgenancy
7. Post-operative

A
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82
Q

When to refer for acute pain

A

Use of acetaminophen/NSAIDs for self-medication of pain should generally not exceed 10 days in adults or 5 days in children, unless directed by a prescriber

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83
Q

Chronic Pain Duration and Differentiation

A

Pain lasting > 3 months
Difference between Chronic cancer pain vs. chronic non-cancer pain

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84
Q

What can chronic pain lead to? Sx?

A

Can lead to a chronic pain syndrome (symptoms/consequences of chronic pain)
Fatigue, ↓ activity, deconditioning
Depressed mood, substance use, suicidal ideation/attempt/completion
Social & financial stress (marital/family/friends, absenteeism, treatment cost)

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85
Q

Chronic Pain Etyiology. Can the exact cause be identified?

A

Often “mixed” pain etiologies (3 categories; overlap between)
Often exact cause cannot be identified

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86
Q

What is chronic secondary pain? Includes?

A

Chronic Secondary Pain:
Diagnosed when pain originally emerges as a symptom of another underlying health condition
May persist even after the underlying condition has been treated, in which case it is considered a disease in its own right

Includes the following sub-diagnoses:
Chronic cancer pain, chronic post-surgical or post-traumatic pain, chronic neuropathic pain, chronic secondary headache, chronic secondary visceral pain, and chronic secondary musculoskeletal pain

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87
Q

Chronic Primary Pain Definition

A

Chronic Primary Pain:

Persists or recurs for longer than 3 months, and
Is associated with significant emotional distress (e.g., anxiety, anger, frustration, depressed mood) and/or significant functional disability (interferes with activities of daily living (ADLs) and participation in social roles), and
The symptoms are not better accounted for by another diagnosis

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88
Q

Gneral Presentation of NEuroptahic Pain

A

Severity may be out of proportion to the degree or severity of the pathology or initial nerve injury

Ongoing nerve damage from persisting factors (e.g., poorly controlled diabetes) can worsen or spread pain over time

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89
Q

Sx of Neuropathic PAin

A

Constant or pulsating pain (shock-like, burning, buzzing, stinging, itching, shooting, radiating [AKA radiculopathy if shooting from lower back down leg(s])
Hypersensitivity to external (e.g., hot/cold, touch) or internal (e.g., anxiety) stimuli
Hyperalgesia: exaggerated pain by normally painful stimulus
Allodynia: pain caused by normally nonpainful stimulus

90
Q

Signs of Neuropathic PAin

A

↓ pinprick sensitivity threshold measured with weighted needles
↓ vibratory sense measured using tuning fork
Slowed peripheral nerve conduction on nerve conduction studies (can be very painful)

91
Q

LAb Tests of Neuropathic PAin

A

Pain is always subjective
Handheld screening devices (e.g. tuning fork) and nerve conduction studies may be used
No specific lab tests but some non-specific tests can indicate nerve conduction issues (e.g. HbA1c, vitamin D, TSH, B12)
History +/- diagnostic proof of past trauma (e.g. CT) may be helpful in diagnosis etiology

92
Q

Nociplastic Pain Gneral

A

Can appear to have no noticeable suffering to complete writhing over pain for all waking hours
Note mental/emotional factors influence pain perception
↓ pain threshold by anxiety, depression, fatigue, anger, fear vs. ↑ pain threshold by rest, mood elevation, sympathy

93
Q

Nociplastic Pain Sx

A

Symptoms may change throughout the day or over time (often occur without a temporal association to an obvious noxious stimuli)

94
Q

Nociplastic PAin Signs,Comorbid Conditions and Tx

A

In most cases, no obvious signs
Some conditions specific (e.g., CRPS - redness, swelling, hair or nail changes in one limb)
Comorbid conditions very commonly present (e.g. insomnia, depression, anxiety) - not always
Outcome of treatment often unpredictable

95
Q

Nociplastic Pain Lab Tests

A

Pain is always subjective
No specific lab tests but history +/- diagnostic proof of past trauma (e.g., CT) may be helpful in diagnosing etiology
No positive lab/diangnostic test for diagnosisng nociplastic pain
General labs may be considered (e.g., vitamin D, TSH, B12)

96
Q

Diagnosis of Nociplastic PAin. Common diagnoses?

A

Best diagnosed based on patient description/history
Common diagnoses: chronic widespread pain syndrome (fibromyalgia), CRPS, TMJ disorder

97
Q

Best pain management uses the….

A
98
Q

What is first line for chronic pain?

A

Non-Pharm
1st line for pain
Essential to long-term success in chronic pain
Individualized recommendations and patient education is key!

99
Q

Goal of Chronic Pain

A

target: functional goals, not complete resolution of pain

100
Q

Role of Continuing Pharmacotx from Acute to Chronic Back LPAin

A

Acetaminophen
Does not appear effective, is not recommended by guidelines
If patient finds benefit, use lowest effective dose (consider max 3200mg/day)
PRN/adjunct use for acute on chronic pain
First choice for people with dementia due to effectiveness in this population and safety

NSAIDs
May be effective for some to manage chronic inflammation causing pain
Lowest effective dose, shortest duration (reassess as risks may > benefits over time)
Non-selective and COX-2 inhibitor comparable efficacy, must consider individualized risk vs benefit
Naproxen and ibuprofen less CV risk
Celecoxib less GI risk (or pair NSAID with PPI or misoprostol if risk factors for bleeding ulcer)
PRN/adjunct use for acute on chronic pain

Muscle Relaxants
No role in chronic pain unless concurrent spasticity (e.g., MS)
Short term use only (< 2 weeks) for acute low back pain
Again, may cause more of a sedative effect than actual relaxant effect

101
Q

Other AGnets for Chronic Low BAck PAin

A

Duloxetine (SNRI) – Health Canada indication
Moderate evidence for benefit in non-neuropathic chronic low back pain
Especially makes sense if concurrent neuropathic symptoms/radiculopathy (i.e., sciatica) or depression or anxiety

Tricyclic antidepressants – not enough evidence for/against
Might be helpful if comorbidities (e.g. chronic migraine, insomnia)

102
Q

Certainity of Evidence of TX Options in Chronic. Low BAck Pain

A
103
Q

Treatment of Low BAck PAin Algorithm(Evidence of Benefit)

A
104
Q

Chronic Low BAck Pain Summary

A

Exercise has consistently been shown to meaningfully improve pain scores and usually improves function, quality of life, and mental health as well

Other “non-pharms” like spinal manipulation and psychotherapy (CBT) have evidence of benefit

Long term NSAID use should be reassessed frequently (~q6-12 months) to ensure benefit still > risks/harms

Duloxetine may be worth considering, may be especially helpful if concurrent GAD, MDD, neuropathic pain
Acetaminophen use is not supported by evidence, but may be trialed

105
Q

Low BAck Pain Summary of Pharmacotx

A
106
Q

Neuropathic Pain TX Summary

A
107
Q

2017 Stepwise Approach for Neuropathic PAinn

A
108
Q

Evidence of Pharmacotx in Neuropathic Pain

A
109
Q

2022 TX of Neuropathic Pain

A

Physical activity less role in neuropathic role – still want to encourage; just may be less benefit than seen in osteoarthritis and chronic low back pain

110
Q

Neuropathic PAin Guidance Bottom Line

A

Consider the patient as a whole and their other medical conditions can you pick a medication that can do “double duty”

Bottom line: inquire about and explore the patient’s medication history and enable them to make the choice

111
Q

Diabetic Neuropathy TX

A
112
Q

Post-Herpetic Neuralgia TX

A
113
Q

Trigeminal Neuralgia Tx.AE, D.I.?

A
114
Q

Examples of Gabapentinoids

A

(gabapentin, pregabalin)

115
Q

MOA of Gabepentinoids

A

Block release of excitatory neurotransmitters by binding to specific calcium channels in the CNS (Structurally similar to GABA but NO effect on GABA neurotransmission)

116
Q

Other indications of gabpentinoids

A

Alcohol withdrawal, anxiety, intractable hiccups, chronic pruritis, focal seizures, restless legs syndrome, perimenopausal vasomotor symptoms

117
Q

Gabapentinoids 1/2 life and elimination

A

5-7 hours (TID-QID dosing)
Excretion is proportional to renal function so dose adjust in renal impairment to avoid accumulation!

118
Q

A/e of Gabapentinoids

A

Dizziness/drowsiness (30%), H/A, N/V, mood changes
Tremor, nystagmus, ataxia, peripheral edema (8%), weight gain (2-3%)

119
Q

D.I. Gabapentinoids

A

No relevant metabolism/CYP effects to consider
CNS depressants and anticholinergics (pharmacodynamic interactions)
Serotonergic agents or potentiators (e.g., mirtazapine, opioids)

120
Q

Gabapentin Elimination, Bioavilability and Dosing Considerations

A

100% renal elimination, no hepatic metabolism

Gabapentin bioavailability is inversely proportional to dose due to saturable absorption, pregabalin has regular PK

Taper off to decrease risk of seizures/withdrawal syndrome
Approx. dose conversion factor gabapentin:pregabalin ~ 6:1

121
Q

How long does it take to see effect of gabapentinoids? How should they be titrated?

A

Gabapentin: Take weeks to see effect

Gabapentinoids can be increased every 3-7 days (1-2 weeks for tolerance) – Can taper quickly (more quickly than medications)

122
Q

TCA Examples

A

amitriptyline [prodrug], nortriptyline [active metabolite], ?desipramine

123
Q

TCA MOA

A

Inhibit the reuptake of serotonin and norepinephrine, block sodium channels, block N-methyl-d-aspartate (NMDA) agonist–induced hyperalgesia

124
Q

Other Indications of TCA’s

A

Depression, insomnia, migraine prophylaxis, interstitial cystitis, IBS, sialorrhea

125
Q

t1/2 TCA’s

A

13-36 hours (once daily dosing HS)

126
Q

A/E TCA’s.C.I?

A

Anticholinergic ADEs (dry eyes, dry mouth, constipation, urinary retention), postural hypotension, sedation, confusion, QT prolongation (baseline ECG if older than 40 or at risk of sudden cardiac death)
Contraindications: MAOI use in past 7 days, severe liver impairment

127
Q

D.I. TCA’s

A

CYP2D6 substrates (major) – amitriptyline
CNS depressants and anticholinergics (pharmacodynamic interactions)
Serotonergic agents or potentiators (e.g., mirtazapine, opioids)
Antiplatelets, NSAIDs (↑ risk of bleeding ulcer)
Bupropion – may lower seizure threshold
Carbamazepine – may lower serum concentration of TCAs
Cyclobenzaprine – TCA-like structure  risk > benefit, ?duplication of therapy

128
Q

TCA Dose, Which agent, and Titration

A

Much lower dose required for pain than depression (1/3 to 1/5 antidepressant dose)
Amitriptyline has been more studied but nortriptyline generally better tolerated
Start at low dose and titrate up slowly, especially in older adults
Taper off to prevent withdrawal

129
Q

Which TCA has less s/e?

A

Notriptylline has less s/e than amitriptyline

130
Q

Titration of TCA’s

A

Increase every 7 days, 2 weeks to ases stolerbaility, 4 weeks as a trial

131
Q

SNRI Examples

A

(duloxetine, venlafaxine [prodrug], desvenlafaxine [active metabolite])

132
Q

MOA of SNRI

A

Inhibit the reuptake of serotonin and norepinephrine at neuronal junctions
Duloxetine also has weak inhibition of dopamine reuptake

133
Q

Other indications of SNRI’s

A

Depression, anxiety, migraine prophylaxis, PMDD, perimenopausal vasomotor symptoms
**duloxetine has some moderate evidence also for chronic low back pain and knee OA

134
Q

t1/2 and excretion of SNRI

A

12 hours (longer in older women) – delayed release particles
Excreted in urine so longer t1/2 in renal impairment (also hepatic impairment for venlafaxine and desvenlafaxine)

135
Q

A/e SNRI’s.Ci?

A

Drowsiness, sedation, constipation, nausea,
hypotension (esp. duloxetine in older women predisposed)
OR increased HR/BP (esp. venlafaxine),
hyponatremia (duloxetine)
Contraindication: MAOI use in past 7 days

136
Q

D.I. SNRI

A

Duloxetine: CYP2D6 inhibitor (moderate) (e.g., will increase aripiprazole, risperidone levels)
Venlafaxine: CYP2D6 inhibitor (weak)
Serotonergic agents or potentiators (e.g., mirtazapine, opioids)
Antiplatelets, NSAIDs (↑ risk of bleeding ulcer)
Smoking (↓ serum concentration of duloxetine)

137
Q

TAper and VEnlafaxine Consideration

A

Venlafaxine inhibits norepinephrine reuptake only at doses ≥ 225mg
Taper off to prevent withdrawal (FINISH)

Flu-like symptoms, Insomnia, Nausea, Imbalance, Sensory disturbances, and Hyperarousal (anxiety/agitation)

138
Q

SNRI’s traget the…..

A

Targeting the descending pathway here

139
Q

How long should SNRI’s be trailed? Where do they work?

A

Targeting the descending pathway here

  • Give 4 weeks of trial
140
Q

Neuropathic PAin Considerations

A

Encourage lifestyle interventions and “non-pharms”, when appropriate
CBT, mindfulness, TENS, acupuncture, mirror therapy, hypnosis, aromatherapy, weighted blankets and other comfort measures, etc.

↑ dose q1-2weeks to minimize adverse effects and assess response
Gabapentin and pregabalin may be titrated faster than this

Generally takes up to 6 weeks once titrated to target/tolerable dose for full analgesic effect of the agent for neuropathic pain

141
Q

Fibromylagia is what type o0f pain?

A

Nociplastic

142
Q

Fibromyalgia Diagnosis

A
143
Q

What is fibormyalgia not?

A

a made-up diagnosis
a diagnosis of exclusion
a mental health or psychosomatic disorder

144
Q

Fibromyalgia SUmmary of Pharmacotx

A
145
Q

Pharmacotx Considerations in Nociplastic PAin

A

Exercise is the most effective treatment, better than any drug

Mind-based treatments also essential

Consider similar approach to comparing non-opioid options indicated for neuropathic pain
Pregabalin, amitriptyline (low dose), duloxetine
Fluoxetine may be considered for CWPS/FM (help on anxiety as symptoms)

Opioids should be avoided in almost all scenarios (can cause hyperactive pain)

Cannabis might be considered if concurrent sleep disturbance, may modulate pain

146
Q

Opiods vs opiates

A
147
Q

Opiod Receptors

A
148
Q

Opiod Indications

A
149
Q

Opiod Dose acute Pain

A

Opiod Naieve

150
Q

Opiod Use Strategies

A
151
Q

Chronic Pain Opiods Advatages/Disadvatages

A
152
Q

Space Trial Findings

A
153
Q

When are IR opiod products used? What is there duration?

A

Used for acute pain, breakthrough pain, or when initiating someone on chronic therapy
Duration ~4-6 hours

154
Q

How often are sustained release opiods dosed? Who are these used in?

A

Q12 hours formulations (q8hrs in select patients)

Q24 hours formulations

Not for acute; harder to take away when initiated, higher doses

155
Q

Buccal Opiods

A

Very short duration (fast in, fast out)
Fentora® (fentaNYL) effervescent tablet
Very long duration (due to slow dissociation from receptor)
Suboxone® tablet & film (buprenorphine - with naloxone)

156
Q

Suppository Opiods Duration

A

Duration ~4 hours
Supeudol® (oxyCODONE)

157
Q

Transdermal Opiods Duration

A

Q72 hours formulation (q48hrs in select patients) – fentanyl patch
Qweekly formulation - Butrans® (buprenorphine) patch

158
Q

What opiods are avilable in injections?

A

morphine, hydromorphone, codeine, fentanyl, Sublocade® (buprenorphine subQ monthly)

159
Q

Difference between IV and Oral

A

Iv s twice as potent

160
Q

When should a control released product not be used?

A

CONTROLLED RELASE – Never acute pain or on an as needed basis

161
Q

What is the reference compound for opiods?

A

Morphine

“Natural” opioid = opiate
“Reference” opioid
Use for conversion factor calculations

162
Q

Morphine Metabolism

A

Metabolized into two primary compounds (excreted in urine)
Morphine-6-glucuronide
Active analgesic
Morphine-3-glucuronide
Not active as an analgesic, CNS stimulation

163
Q

Morphine Monitoring

A

Monitor closely (or avoid) if CrCl <20-30 mL/min
Accumulation of metabolites may lead to toxicity
Monitor for CNS toxicity (confusion, ↓ LOC), if occurs change to alternative opioid
If long-term opioid required consider alternative in patients with CKD

164
Q

Codeine Comparison to Morphine and MEQ

A

Much less potent than morphine
MEQ= 0.15
200mg of oral codeine ≈ 30mg of oral morphine

165
Q

Codeine Metabolism.Issue with metabolism?

A

Prodrug - Converted to morphine in the body via CYP2D6
Conversion required for analgesic effect
~10% of population is deficient in CYP2D6 = no pain relief
Ultra-rapid metabolizers = ↑ adverse drug effects
Due to higher morphine exposure

166
Q

Codeine Drug Interactions and CAutions

A

Potential drug interactions with agents that inhibit CYP2D6 = less pain control
Caution in breastfeeding/chestfeeding
rapid metabolizers  ↑ morphine toxicity risk in infant

167
Q

CAse STudy of Codeine

A

CYP2D6 metabolism of codeine to morphine is a minor pathway of codeine metabolism (<10%)

Ultra-rapid metabolizers have higher conversion to morphine

Case describes codeine toxicity due to ultrarapid CYP2D6 metabolism, CYP3A4 inhibition, renal failure

168
Q

Codeine C.I.

A

Contraindications:
< 12 years old, < 18 years old post op tonsillectomy and/or adenoidectomy

169
Q

What formulations of codeine are avilable?

A

Available by itself or in combination with acetaminophen and caffeine (other combo products available)

170
Q

ANti-tussive Dose of Codeine

A

Antitussive at dose > 15mg q4-6h

171
Q

Oxycodone MEQ

A

~1.5x more potent than morphine
20mg of oral oxycodone ≈ 30mg of oral morphine

172
Q

Oxycodone Metabolism

A

Metabolized by CYP3A4 (major) and 2D6 (minor) to active metabolites
↑ ADE if ultra-rapid metabolizer

173
Q

Avilable Formulation of Oxycodone

A

OxyContin
Brand discontinued in 2012; route easily altered
Crushed, chewed, snorted, injected

OxyNeo
Bioequivalent to OxyContin
Formulation is different
Forms a viscous gel when wet
Difficult to break the tablets
If broken, the broken pieces still retain some controlled release formulation

174
Q

Oxycodone Combo Products

A

acetaminophen 325mg and oxycodone 5mg (brand name formerly Percocet)

ASA 325mg and oxycodone 5mg (brand name formerly Percodan)

Targin (oxycodone + naloxone)

Naloxone = “opioid antagonist that competes and displaces opioids at opioid receptor sites, including gut opioid receptors, which counteracts opioid-induced constipation” - Limited evidence, no better than opiod with laxative

175
Q

Hydromorphone MEQ. A good option when….

A

Synthetic opioid
5 times more potent than morphine
1mg of oral hydromorphone ≈ 5mg of oral morphine
Good option if require an opioid in renal impairment

176
Q

Tramadol MOA

A

Dual mechanism of action
Mu receptor agonist
Inhibits serotonin and norepinephrine reuptake

177
Q

Tramadol MEQ

A

Binding affinity for mu receptor is ~600 times less than morphine
100mg of oral tramadol ≈ 10-20mg of oral morphine (rough estimate)

178
Q

Tramadol Metabolism

A

Prodrug - Metabolized to active metabolite via CYP2D6
O-desmethyl tramadol

179
Q

Tramadol Risks

A

↑ risk of seizures, serotonin syndrome (more likely), hypoglycemia, QT prolongation

180
Q

Tapentadol

A

Tapentadol – More potent than tramadol, but less potent than morphine

181
Q

Tramadol and Tapentadol Dosing Unique

A

Max recommended dose – sertonergic and norepeinephrine effects

182
Q

Fentanyl MEQ. With the formulation avialble of fentanyl, how is this converted?

A

Much more potent than morphine (~100x)
25mcg/hour patch ≈ 100mg of oral morphine

This is a DAILY equivalent

This does NOT mean 100mg of morphine equivalency is released per hour

LOTS of controversy regarding this conversion

Conversion is safe when converting from opioid to fentanyl patch BUT
Conversion is aggressive when converting from fentanyl patch to other opioid (TABLE NOT MEANT TO BE USED )

183
Q

Fentanyl Patch USed for….

A

Option for those who cannot take oral medications & who are opioid-tolerant

184
Q

Opiod Tolerance Definition

A

someone taking 60 MEQ for a week to be opiod tolerant

185
Q

How often is the fentanyl patch dosed?

A

Dosing schedule of q72hours
Considered convenient
Also may be considered/inconvenient, ?forgetfulness

186
Q

Fentanyl Metabolites

A

No known active metabolites
Option for patients with renal impairment

187
Q

Fentanyl patch not suitable for….

A

Diaphoresis
Morbid obesity
Ascites
Cachexia (wasting of the body)

Also parenteral formulation

188
Q

If patch touches skin during application?

A

If gel from the patch contacts your skin (e.g., hands) during the application procedure, wash with water only and not soap, as soap will increase the absorption of the patch through the skin

189
Q

What dose of the patch should be used for alterations? Fentanyl Patch Alterations

A

Use the 12mcg/hr patch for dosing titrations / tapers

If required, can cover half of the area of a patch with an occlusive dressing/barrier
NOT officially recommended
Area covered is the patch-skin interface (do not cover the whole patch- ↑ absorption, risk of toxicity)

Matrix membrane patch = technically could be cut
NOT officially recommended, inaccurate dosing
Monograph indicates the patch should not be cut

190
Q

Methadone MOA

A

Potent mu (μ) opioid receptor agonist and an NMDA (N-methyl-D-aspartate) receptor antagonist

NMDA mechanism plays a role in prevention of opioid tolerance, potentiation of analgesic effects, & neuropathic pain treatment

191
Q

Methadone Half Life and Riskwith half-life? When should dose adjustments be made?

A

Long and variable half-life: ~10-60 hours (24-190hrs for some)
Potential for accumulation and overdose
Do not increase dose more frequently than q3-5days

192
Q

Methadone:How long does the analgesia last for? How often is it dosed?

A

Observed duration of analgesia 6-12 hours
Usually dosed q8h for pain (occasionally q6-12h). Differs from once daily dosing for opioid use disorder.

193
Q

Is methadone equivalent to other opiods? Caution in? Can metahdone equivalence be converted to other opiods?

A

Equianalgesic potency compared to other opioids is unpredictable

Caution in severe hepatic failure, hepatitis, concurrent antiretroviral use

Various published guidelines to convert morphine  methadone but not from methadone  other opioids

194
Q

Methadone Renal Impairment

A

Useful in renal impairment because inactive metabolites are excreted in the urine and feces

195
Q

Methadone Risksand Management of Risk

A

Risk of QTc prolongation
Initiating prescribers should generally obtain an ECG at baseline

Additional ECG if:
dose >100mg
after every ↑ of 20 mg
unexplained dizziness or fainting
Initiation of additional QT prolongation medication

↑ risk of serotonin syndrome when combined with serotonergic drugs

196
Q

Methadone: Why should dose adjustments only be made every 5 days? What ahppens if you stop it abruptly?

A

Slow onset = progression of respiratory depression is insidious (come on before you know it)

24 h t1/2; serum levels will ↑ with each dose until steady state is reached (4-5 half lives)
= ↑ risk of overdose and death

Prescribers should not increase dose more frequently than every 5 days

Physiological dependence  physical and psychological withdrawal symptoms if discontinued abruptly

197
Q

Buprenorphine for Pain Formulations, Dose and Titration

A

Buprenorphine (BuTrans)
Patch formulation for persistent, moderate pain
Non-formulary
Applied q7days

Opioid naïve patients
Start with 5mcg/hr q7d
Can increase after 7 days (no sooner than 3)
Max. 20mcg/hr

198
Q

Buprenorphine Roptation from Other Opiods

A

Buprenorphine dose in BuTrans is relatively low (even at max of 20mcg/hr)

Can only convert relatively low doses (< 90 MEQ) of other opioids to Butran patch

  • More than 90 MEQ cannot switch to patch – use buprenorph/naloxone sublingual
199
Q

Buprenorphin MOA. Advantages?

A

Receptor Interactions: mu-partial agonist, delta & kappa antagonist

Analgesia, decreased opioid-induced hyperalgesia & tolerance
Better safety profile
May cause less anxiety & depression

200
Q

Buprenorphine t1/2.Benefits?

A

High affinity, slow dissociation, long elimination half-life (~37hrs subling tab)
More consistent serum concentrations, can alleviate end-of-dose withdrawal
Flexibility in dosing schedules

201
Q

Buprenorphine Metabolism.Renal and Hepatic Dysfx?

A

Metabolism: CYP3A4 substrate (major)
Safe in decreased renal function
Relatively safe with hepatic dysfunction (may ↓ dose if severe impairment)

202
Q

Opiod Contraindications

A

Allergy

Co-administration of a drug capable of inducing drug-drug interaction

Active diversion of controlled substances

203
Q

Opiod Alllergy. Management

A

Rare

204
Q

A/e of Opiods

A

Sedation
Respiratory depression
Constipation
Nausea
Miosis (pinpoint pupils)
Itching / rash (pseudoallergy)
histamine release from cutaneous mast cells, not a true allergic or immunoglobulin-E (IgE) or T-cell response (see last slide)

Too much opiods – miosis
Withdrawl – pupils get wider

205
Q

Do patients develop tolerance to opiod adverse effects? When does this occur?

A

Patients will develop tolerance to all adverse effects of opioids except constipation and miosis (pin-point pupils)

Tolerance to respiratory depression:
Tolerance to respiratory depression can be lost quickly within 1 -2 days of no opioids  high risk for overdose if return to previous dose!

Tolerance to sedation:
Begins after 3 to 4 days
May take up to 10 days
Highly variable, may never resolve

206
Q

Long-term Side Effecrs of Opiods

A

General adverse effects of opioids (develop over the longer term, even as short as weeks):

Hypogonadism
Sleep apnea
Opioid-induced hyperalgesia
Opioid tolerance
Opioid dependence, opioid use disorder
Risk of opioid toxicity (overdose) multifactorial

207
Q

Opiod Drug Interactions

A
208
Q

Hypogonadism Mechanism of OPIODS

A

Opioids influence the hypothalamic-pituitary-adrenal axis and the hypothalamic-pituitary-gonadal axis

Morphine has been reported to cause a strong, progressive↓ in the plasma cortisol level

Opioids interfere with the modulation of hormonal release, including:
an ↑ in prolactin
a ↓ in luteinizing hormone, follicle-stimulating hormone, testosterone, and estrogen

Testosterone depletion has been demonstrated in people with opioid (heroin) use disorder and in patients receiving methadone maintenance therapy

The collective effects of the hormonal changes may lead to ↓ libido and drive; aggression; amenorrhea or irregular menses; and galactorrhea

209
Q

Sleep Apnea Opiods

A

Patients on long-term sustained-release opioids show a distinctive pattern of sleep-disordered breathing called central sleep apnea that is different from the disturbances usually observed in people with obstructive sleep apnea (OSA)

The oxygen desaturation is more severe and respiratory disturbances are long during NREM sleep

Opioids may complicate underlying sleep apnea and make continuous positive airway pressure (CPAP) therapy less effective

210
Q

Opiod Tolerance.What can it result in?

A

May have decreased effect over time

Withdrawal-mediated pain is becoming increasingly understood

Mechanism still unclear

May result in end-of-dosing interval increase in pain
Beyond underlying pain severity

211
Q

Opiod Induced Hyperalgesia.What is its mechanism?

A

↑ sensitivity to pain

Even after one month of opioid therapy in patients with chronic pain, hyperalgesia has been documented

Opioid-induced hyperalgesia appears to be more likely with higher doses of opioid, for longer periods of time

Mechanism of OIH is unclear but speculated to be related to NDMA receptor sensitization, increased glutamate release, and immune cell changes (e.g., microglial and glial cells)

212
Q

Opiod Induced Hyperalgesis Management

A

Consider dose reduction (tapering), opioid rotation (account for cross-tolerance), rotation to buprenorphine or methadone

213
Q

Risk of opiod use disorder associated with:

A

History of substance use disorder (SUD),
Taking opioids for >90 days, or
Taking higher doses (>120 MED)

214
Q

Opiod USe Disorder Screening

A

POMI
Score > 2 = positive screen
COMM
Score > 9 = positive screen

215
Q

Opiod USe Disorder MAngement

A
216
Q

Signs of Overdose

A

Difficulty
walking
talking
staying awake

Blue lips or nails
Very small pupils
Cold and clammy skin
Dizziness and confusion
Extreme drowsiness
Choking, gurgling, or snoring sounds
Slow, weak or no breathing
Inability to wake up, even when shaken or shouted at

217
Q

Response to Overdose

A

If you think someone is overdosing, call 9-1-1 ASAP

Give naloxone (if available)

An overdose is always an emergency
Naloxone may wear off before overdose completely resolved
Additional doses may be required
Always call for help

218
Q

Naloxone mOA

A

Binds the same sites as opioids in the brain (more tightly)
Displaces opioid
Antagonist at receptor

Restores breathing within about 2 to 5 min when it has been dangerously slowed or stopped due to opioid use

219
Q

Admin Naloxone

A

IM:
Can be given through clothing into the muscle of the upper arm or upper leg

220
Q

Cautions of NAloxone

A

Can cause opioid withdrawal in those with opioid dependence
Benefit > risk

Effects wear off after 30- 90 min, so overdose may return
Especially if patient was taking long-acting opioid (e.g. methadone)

221
Q

Management of acute on chronic pain

A

Challenging due to opioid tolerance & potential hyperalgesia
Educate patient
Pain relief aimed at acute pain
Maintain analgesia for underlying pain condition
May use short acting opioids for new ACUTE pain
May require 2-3x higher dose than an opioid naïve patient
Use adjuvant analgesics
Acetaminophen, NSAIDs, ketamine, gabapentinoids
Return to prior analgesic dose when acute pain resolved

PHAR 255 Exam 2 (5 decks)

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