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301 Pain Flashcards

1
Q

Describe the pain pathway and relevant neurotransmitters

A

Stimulus: Noxious input activates C-fibers
Releases mediators (e.g., BK, 5-HT, PGs), NGF, and neuropeptides (SP, CGRP)
Excites neurons that carry pain signals to the brain
Enkephalins and GABA further inhibit pain transmission
Key Neurotransmitters: 5-HT, NA, enkephalins, GABA

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2
Q

What do opioids do in the pain pathway?

A

Endogenous/exogenous opioids inhibit pain signals

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3
Q

What happens in descending pain pathway?

A

Serotonin (5-HT) and noradrenaline (NA) reduce pain perception

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4
Q

Nociceptor structure

A

Cell body with cross section of spinal cord including peripheral terminal (somatic, visceral) and central terminals (spinal cord dorsal horn, brainstem)

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5
Q

Types of fibers in the peripheral nerves

A

Aδ Fibers: thin, myelinated fibers; transmit sharp, fast pain (acute pain)
C Fibers: unmyelinated fibers, carry dull, slow pain (chronic pain)
Aβ Fibers: thick, myelinated fibers, transmit touch & pressure, can inhibit pain when stimulated (e.g., rubbing a sore area)

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6
Q

What is the difference between Aδ and C fibers and Aβ fibers?

A

Aδ and C fibers carry pain while Aβ modulates it

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7
Q

What activates nociceptive neurons, and how is pain signal transmitted?
Activation
Release of mediators
Response pathway
Transmission to CNS

A
  1. Heat, cold, pressure, & tissue injury stimulate nociceptive neurons in the periphery
  2. Injured tissues release substances like bradykinin, prostaglandins, ATP & H+ ions
  3. Mast cells or neutrophils release histamine & Substance P
    CGRP & Substance P cause vasodilation in blood vessels
    Nerve Growth Factor (NGF) and serotonin (5-HT) contribute to pain signal
  4. Signals travel to the dorsal root ganglion (DRG), spinal cord & higher brain centres, creating sensation of pain
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8
Q

How is pain transduced from stimulus to action potential in nociceptive fibres?
Overview
Aβ-fiber
Aδ-fiber
C-fiber

A
  1. Stimulus activates mechanoreceptors or channels, creating a generator potential, which leads to an action potential
  2. Mechanoreceptors trigger Na+ influx via voltage-sensitive sodium channel
  3. Responds to histamine & bradykinin (BK) through H1 & K+ channels
  4. Responds to noxious stimuli through VR1 receptors, allowing Ca2+ & Na+ influx
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9
Q

What stimuli trigger each of the peripheral nerve fibers?

A

Aβ - non-noxious mechanical stimuli
Aδ - noxious mechanical stimuli
C - noxious heat and chemical stimuli

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10
Q

What are the main transducers in nociceptors, and how do they relate to pain perception?
Heat (Capsaicin)
Cold (Menthol)
Acidic environments
Mechanical sensitivity (pressure)
Pathway
Result

A
  1. Activates TRPV1 receptors
  2. Activates TRPM8 receptors
  3. Stimulate ASIC & DRASIC receptors
  4. Activates MDEG, DRASIC, TREK-1
  5. Activation of NaV1.7, 1.8, 1.9 channels generates an action potential
  6. Signal travels through the dorsal root ganglion to the spinal cord & brain, leading to pain sensation & withdrawal or emotional reactions
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11
Q

First and second pain: hand on hotplate example

A
  1. Immediate, sharp, localised pain, transmits by A-delta fibers (myelinated), alerts you to move hand preventing further harm
  2. Slower, duller pain, transmits by C fibers (unmyelinated), sensation lingers with prolonged discomfort, reminder of injury to not re-injure whilst healing
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12
Q

What happens when nociception arrives in spinal cord?

A

Dorsal horn of spinal cord receives nociceptive signals
Integration & transmits information to CNS regions

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13
Q

Pain modulation mechanism theory of pain: Cartesian model of pain

A

This does not explain the whole story: things are more complex that this picture shows
Complexity cannot be explained by a simplistic relationship between peripheral and CNS

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14
Q

Pain modulation mechanism theory of pain: gate theory of pain

A

(Attempted to explain some complexity)
C-fibre nociceptor signal are inhibited at spinal cord level by large nerve fibres (A-alpha, A-beta) before they are transmitted to brain & perceived as pain

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15
Q

Gate theory of pain in practise:
TENS (Transcutaneous Electrical Nerve Stimulator)
Physical therapies (principal of counter-stimulation)
Spinal cord stimulators

A
  1. Used for labour or low back pain
  2. Heat, cold massage, manipulation & acupuncture
  3. Patients with chronic pain when other methods fail, same principle as TENS
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16
Q

Descending modulatory system

A

Descending nerve pathways from brainstem, inhibits facilitate nociceptive signals in spine
Implies pain perceived in brain can be decreased or increased
Hence modification of gate theory to include descending nerves

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17
Q

What neurotransmitters are involved in descending modulation?

A

Opioids
Serotonin (5HT)
Noradrenaline
Gamma amino butyric acid (GABA)

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18
Q

Bidirectional pain network

A

Noxious signal being modulated at several levels between spinal cord and brain
1. Cognition
2. Mood
3. Experience
4. Attention

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19
Q

Types of nociceptive pain

A

Somatic - well-localised, pain receptors in soft tissue, skin, skeletal muscle & bone
Visceral - vague, visceral organs
Neuropathic - damaged sensory nerves

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20
Q

What is nociceptive pain?

A

Response to pathophysiological process occurring in tissues (inflammation)
Pain signal originates in primary afferent nerves signalling noxious events

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21
Q

What are nociceptors?

A

Pain activated by agents like prostaglandins, bradykinin, serotonin, adenosine & cytokines

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22
Q

What is neuropathic pain?

A

Signals generated ectopically without ongoing noxious activity from pathologic route in peripheral or CNS

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23
Q

Pain classification

A

Duration, intensity, presumed pathophysiology (visceral, somatic, sympathetic), opioid sensitivity, pragmatic

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24
Q

Practical pain classification

A

Neuropathic - disordered sensation - anticonvulsants & antidepressants
Bone - intense & focal - NSAIDS & bisphosphonates
Muscle spasm - muscle relaxants & antispasmodics
Cerebral irritation - caused by brain injury, sign of anxiety - BZDs

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25
Q

Pain control mechanisms

A

Aspirin and NSAIDS
Morphine and opioids/cannabinoids
TENS
Deep brain stimulation
Placebo
Acupuncture
Hypnosis

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26
Q

Anatomy of pain pathway

A

Primary afferent neuron –> dorsal root ganglion —> second order neurons –> to brainstem and thalamus

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27
Q

WHO pain ladder and analgesics

A

Step 1. non opioid (paracetamol)
Step 2. weak opioid (codeine mild/moderate pain) + non opioid
Step 3. strong opioid (morphine for moderate/severe pain) + non opioid

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28
Q

WHO cancer pain ladder for adults

A
  1. Non opioid +/- adjuvant (paracetamol & NSAIDS)
  2. Opioid for mild to moderate pain +/- non-opioid & +/- adjuvant (codeine, dihydrocodeine & tramadol)
  3. Opioid for moderate to severe pain +/- non-opioid & +/- adjuvant (morphine, diamorphine, buprenorphine, fentanyl & oxycodone)
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29
Q

What is the afferent and efferent neuron?

A

Afferent - sensory
Efferent - motor

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30
Q

What can anti-inflammatory medication inhibit in the pain pathway and what does it cause?

A

NSAIDs can inhibit release of mediators like prostaglandins, reducing inflammation & pain

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31
Q

What do the ascending and descending pain pathways do?

A

A: transmits pain signals to brain
D: modulate and inhibit signals to manage pain perception

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32
Q

What takes place in the ascending pain pathway?

A

Pain signals travel from C and Aδ fibers in spinal cord brain
Signals pass through medulla, pons & midbrain
They reach the thalamic nuclei and forebrain, processing “early pain” (sharp, initial pain) and “late pain” (dull, prolonged pain)
Reticular formation & periaqueductal gray are involved in pain perception

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33
Q

What takes place in the descending pain pathway?

A

Pain modulation starts in the frontal cortex, hypothalamus, and periaqueductal gray
These pathways involve locus coeruleus, raphe nuclei, and medulla, releasing inhibitory signals
Signals descend to the spinal cord, reducing pain transmission from skin & other areas

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34
Q

Summary of entire pain pathway:
Site of injury
Spinal cord
Brainstem
Cerebrum

A
  1. Pain begins with injury stimulating unmyelinated C-fibers & myelinated Aδ fibers, detect & transmit pain signal
  2. signal travels along afferent nerves to spinal cord, where synapses & ascends via spinothalamic tract
  3. Signal moves through brainstem, including reticular formation & midbrain, where modulated
  4. Signal reaches thalamus & relayed to cerebral cortex for perception, allowing individual to feel & localise pain
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35
Q

Definition of pain

A

An unpleasant sensory & emotional experience associated with, or resembling that associated with, actual or potential tissue damage

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36
Q

Major features of pain experience

A

Sensory discriminative
Affective (emotional)
Cognitive

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37
Q

What is nociception?

A

Nociception is neural process of encoding noxious stimuli, it is triggered when noxious stimuli act on specialised peripheral nerve endings

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38
Q

What can occur in nociception?

A

It does not necessarily result in individual perceiving pain
It also possible for an individual to perceive pain when there is no nociception, occurs in some chronic pain states

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39
Q

Types of pain

A

Acute, chronic, malignant vs nociceptive, neuropathic

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40
Q

What are the 3 basic causes of pain?

A
  1. Acute trauma or injury
  2. Chronic painful conditions for which cures were unknown
  3. Malignant processes (cancer and arthritis)
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41
Q

What 2 types of pain are shown in modern research?

A

Nociceptive pain
Neuropathic pain

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42
Q

Where is the cell body located in nociceptors

A
  • Dorsal horn of spinal cord
  • Vagus nodose ganglion
  • Trigeminal ganglia
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43
Q

What is a nociceptor?

A

Peripheral sensory terminal (part that senses noxious stimulus)
A central termination within spinal cord or brainstem

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44
Q

What activates nociceptors?

A
  1. Physical trauma
  2. Chemicals
  3. Excessive heat or cold
  4. Stretching beyond normal range, which can trigger nociception in muscle
  5. Ischaemia (insufficient blood flow) e.g. angina and inflammation also causes pain
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45
Q

What is capsaicin?

A

Gives chilli peppers their heat, may help wound healing by reducing inflammation

46
Q

What are A-alpha/A-beta fibres in nociception?
What type of nociception?
What type of structures are they?
What are the terminals associated with? Transmission speed?

A

Mechanical & thermal nociception
Innervate somatic structures
Terminals associated with specialised sensory structures
Proprioceptive (skeletal muscle, tendon organs), mechanosensitive (light touch)
Very fast (30-120 m/s)

47
Q

What are A-delta fibres in nociception?
What type of nociception?
What type of structures are they?
What type of nerve endings?
Transmission speed?

A

Mechanical, thermal & chemical
Innervate somatic & visceral
Specialised or free
Mechanosensitive (stretch & touch skin, viscera)
Thermosensitive
Fast (4-30m/s)

48
Q

What are C fibres in nociception?
What type of nociception?
What type of structures are they?
What type of nerve endings?
Transmission speed?

A

Mechanical, thermal & chemical
Innervate somatic & visceral
Free nerve endings
Mechanosensitive (stretch & touch)
Thermosensitive
Chemically sensitive (itch)
Slower <2.5m/s

49
Q

Natural products and what can they treat?
Capsicum (TRPV1)
Mentha (TRPM8)
Brassica (TRPA1)
Allium (TRPA1)

A
  1. Heat
  2. Cold
  3. Pain
  4. Pain
50
Q

Cross section of peripheral nerve fibres:
Aβ
Aδ
C

A
  1. Large myelinated fibres (response e.g. to light touch, joint movements)
  2. Small myelinated fibres
  3. Unmyelinated fibres: these conduct very slowly & most of them are those that are involved in generating pain message
51
Q

What is the first and second type of pain and what are the signals carried by?

A
  1. Sharp & brief, myelinated Aδ neurons
  2. More delayed & longer lasting, feels more dull, thin & unmyelinated C fibres
52
Q

What are the 2 possible outcomes when nociception arrives in the spinal cord?

A
  1. Can trigger reflex activity like hotplate example - occurs within spinal cord
  2. Convey information to brain regarding location & intensity of stimulus
53
Q

Function & contribution to pain perception:
Somatosensory cortex
Limbic system
Prefrontal cortex

A
  1. Sensory discrimination & localises site, quality and intensity of stimulus
  2. Affective-motivational function & emotional aspects of pain, attention to & memory of pain
  3. Cognitive evaluation of pain & executive control of purposeful behaviour, emotion, memory and decision making
54
Q

What is somatosensation?

A

Sense of touch, or the ability to perceive stimuli related to temperature, pressure, pain, body position, and balance

55
Q

What is proprioception?

A

Sense of body position and movement

56
Q

What is nociception?

A

Process by which the central and peripheral nervous systems (CNS and PNS) process harmful stimuli, such as tissue damage or extreme temperatures

57
Q

What is acute pain?

A

Sudden, sharp pain that’s usually caused by an injury, illness, or other environmental stress

58
Q

What is chronic pain?

A

Pain that lasts longer than the typical recovery period or occurs along with a chronic health condition

59
Q

What is neuropathic pain?

A

Nerve pain that can happen if your nervous system malfunctions or gets damaged

60
Q

What is allodynia?

A

A condition where a stimulus that normally wouldn’t cause pain results in pain

61
Q

What is noxious stimulus?

A

Physical change that can be internal or external and is strong enough to potentially damage tissue or threaten the body’s integrity

62
Q

What is sensitisation?

A

Process that occurs in the nervous system and a type of non-associative learning

63
Q

What is central sensitisation?

A

Condition where the central nervous system (CNS) becomes hypersensitive to pain and other sensory stimuli

64
Q

What is hyperalgesia?

A

An increased sensitivity to pain or an extreme response to pain

65
Q

What is the dorsal root ganglion?

A

Neural structure in the spinal column that plays a key role in processing and developing chronic pain

66
Q

What are projection neurons?

A

Neurons in the central nervous system (CNS) that send axons from their cell bodies to other regions of the CNS

67
Q

What is the spinothalamic tract?

A

Sensory pathway in the nervous system that carries information about pain, temperature, touch, and pressure from the skin to the brain

68
Q

What are the spinobulbar tracts?

A

Pathways that carry information up and down the spinal cord between brain and body

69
Q

What is the somatosensory cortex?

A

The part of the brain that receives and processes sensory information from the body, such as touch, temperature, and pain

70
Q

What is analgesia?

A

Pain relief or absence of pain

71
Q

What is musculoskeletal pain?
Conditions

A

Damage to bones, joints, muscles, tendons, ligaments etc
Osteoarthritis (OA), rheumatoid arthritis, lower back pain

72
Q

What is osteoarthritis?

A

Clinical syndrome of joint pain accompanied by varying degrees of functional limitation & reduced QoL
Most common form of arthritis and 1 of leading causes of pain & disability worldwide

73
Q

NICE guidance for osteoarthritis treatment

A
  • Offer topical NSAIDs to people with knee OA
  • Do not routinely offer paracetamol or weak opioids unless used infrequently for pain relief & other treatment C/I
  • Explain to OA patients no strong evidence of paracetamol benefit
74
Q

Osteoarthritis diagnosis

A

Diagnose clinically without investigations if person is 45+ and has…
- Activity-related joint pain
- Either no morning joint-related stiffness or morning stiffness no longer than 30 mins
- Differential e.g. gout, RA, malignancy

75
Q

Assessing pain:
Numerical rating scale
Visual analogue scale

A
  1. Mark on scale of 0 (no pain) to 10 (worst) how strong it is
  2. Mark on 10cm line with no pain at one end and worst pain at other
    Mild: 3/10
    Mild to moderate: 3-6/10
    Severe: 6/10
76
Q

Non-pharmacological management of osteoarthritis

A
  • Exercise: muscle strengthening & aerobic fitness
  • Weight loss
  • TENS
  • Neutraceuticals: no glucosamine/chondroitin
  • Acupuncture: no
  • Manipulation & stretching
  • Aids & devices
77
Q

WHO pain ladder:
Step 1
Step 2
Step 3

A
  1. Simple analgesics e.g. aspirin & paracetamol
  2. Opioids suitable for mild to moderate pain use & simple analgesics
  3. Opioids suitable for severe pain use & simple analgesics
78
Q

Paracetamol pharmacology

A
  • Analgesic & antipyretic
  • Little or no anti-inflammatory activity (not considered NSAID)
  • MOA unknown (weak inhibitor of COX1 and COX2, possible greater effect in CNS)
  • Very minimal GI irritation
  • No effect on bleeding time
  • No effect on respiration
  • Not uricosuric
79
Q

What are anti-pyretic and uricosuric meanings?

A
  1. Reduces fever by tricking hypothalamus into overriding temp caused by prostaglandins
  2. Drugs that promote uric acid secretion
80
Q

NSAIDs pharmacology

A
  • Analgesic, antipyretic, anti-inflammatory
  • Inhibit peripheral prostaglandin synthesis
  • Prostaglandins implicated in pathogenesis of fever & inflammation
  • Inhibit cyclo-oxygenases (inhibition of COX2 = therapeutic effect, COX1 = adverse effects)
  • COX2 selective/COX2 specific NSAIDs (Coxibs)
  • Standard NSAIDs = non selective
81
Q

NSAIDs indication

A
  • Fever
  • Inflammation
  • Mild/moderate pain
  • Musculoskeletal pain
82
Q

What do COX1 and 2 do?
Important products
Inhibition

A
  1. metabolise arachidonic acid
  2. Prostaglandins E2, D2, F2, A2 and I2 (prostacyclin)
  3. Non-selective NSAIDs block both COX1 and 2 enzymes
    Selective COX2 inhibitors specifically target COX2 without affecting COX1
83
Q

Diclofenac and ratio (COX2:COX1 50% inhibition)

A

Diclofenac is COX2 selective with a ratio of 0.05

84
Q

Opioid analgesics pharmacology

A

Opioid - morphine like effects
Opiate - morphine & codeine
Agonists at opioid receptors
- Morphine, diamorphine, oxycodone, codeine
- Pethidine & fentanyl
- Buprenorphine

85
Q

Opioid analgesics:
Codeine/dihydrocodeine
Tramadol

A
  1. Pro-drug - metabolised to morphine (5-10% population lack gene)
    MOP agonist (+KOP & DOP)
    Mild pain
  2. Weak agonist
    Inhibits MAO
86
Q

Effects of opioid receptor stimulation

A

Analgesia
Respiratory depression
Pupil constriction
Reduced GI motility
Euphoria
Hallucinations
Sedation
Catatonia
Dependence

87
Q

Analgesic efficacy in osteoarthritis:
Short term
Moderate term
Long term

A
  1. NSAIDs (oral & topical) offer robust relief
  2. Duloxetine for several months
  3. Limited (NSAID or opioid use generally avoided due to risks), non-pharmacological approaches
88
Q

Topical NSAIDs vs placebo efficacy

A

Topical NSAIDs superior for 1st 2 weeks but not following 2 weeks

89
Q

Topical NSAIDs and topical capsaicin

A
  1. More efficacious than placebo, trial evidence is poor, evidence suggests ineffective after 2 weeks to 1 month use
  2. More efficacious than placebo
    Not tolerated in 1/3 patients
90
Q

NSAID effectiveness

A

No important differences in efficacy between NSAIDs
Benefits of NSAIDs increase towards max. value at high dose
No ceiling for adverse effects which increased in approx. linear fashion with dose
(Consider individual response, some patients need to try different NSAIDs)

91
Q

Tramadol in osteoarthritis

A

Codeine should be tried first
Profile for tramadol similar to codeine (but more SEs, now a CD)
Some evidence of effectiveness in OA

92
Q

Paracetamol side effects

A
  • Overdose = liver toxicity due to glucuronide conjugation saturated & mixed function oxidase metabolism (2ndary pathway) produces highly reactive free radicals
  • Hepatic necrosis occurs after 10-15g dose, >25 fatal
  • Increased hepatotoxicity taken with alcohol or due to alcohol inducing MFO pathway or while fasting (4g/day)
  • Nephrotoxicity - renal tubular necrosis, increased risk if lifetime in take >1000 tablets
93
Q

NSAID ADRs

A

Upper GI bleed 18 per 100,000
Acute renal failure 10 per 100,000
Congestive heart failure 22 per 100,000

94
Q

NSAIDs main side effects

A

GI side effects, dyspepsia, ulceration, bleeding
Indomethacin = more common
Ibuprofen = less common

95
Q

What 3 drugs have high COX2 selectivity?

A
  1. Rofecoxib (Vioxx)
  2. Etodolac (Ultradol)
  3. Celacoxib (Celebrex)
96
Q

GI side effects: influencing factors with NSAIDs

A

Type of NSAID (COX2 selectivity, half-life, acidity)
Current vs past vs never use
Duration of use
Dose
Hx of PUD
Age of patient

97
Q

NSAID renal side effects

A

Renal perfusion depends on prostaglandins (cause vasodilation, opposing vasoconstriction of NA & angiotensin II)

98
Q

NSAIDs CV side effects

A

Patients with CHF, chronic renal disease (NSAIDs decrease renal blood flow & GFR, creatinine clearance may fall up to 50%)
Promote salt & water retention (reduce PG inhibition of both chloride re-absorption & ADH action, may cause oedema, oppose anti-hypertensive action)
Promote hyperkalaemia by PG renin secretion suppression, enhance reabsorption of K+ due to decreased availability of Na+ at distal tubular sites
May progress to irreversible renal insufficiency

99
Q

Other side effects of NSAIDs:
CNS
Ocular
Others

A
  1. Dizziness, lightheadedness, headache (indomethacin = severe frontal headache)
  2. Blurred vision, corneal opacity (indomethacin)
    Reversibly prolong bleeding time
    Cross hypersensitivity with aspirin (worsening of asthma (CSM warning))
    Skin rash
    Weight gain
100
Q

Why do COX2’s have adverse CV effects?

A
  1. Within endovascular lumen platelet COX1 dependent prothrombotic (TXA2) & endothelial COX2 dependent antithrombotic (PGI2) are balanced so prevent coagulation
  2. Selective COX2 inhibitors impair PGI2 synthesis but lack antiplatelet effects, tipping scales in favour of relative increases in TXA2, thrombogenesis & increasing CV event risk
101
Q

Why do vets want to ban diclofenac?

A

1.In India Gyps Vulture experience fastest decline in any bed - 95% in 10 yrs
2. Vultures eat dead cattle bodies
3. Diclofenac extensively used in cattle
4. Birds dying from renal failure

102
Q

NSAID CV adverse effects:
Coxibs
Diclofenac

A
  1. Cause small increase of thrombotic effect risk compared to placebo, estimated 3 per 1,000 for one year on average, all coxibs C/I in IHD patients, peripheral arterial disease and/or CV disease
  2. Diclofenac 150mg has thrombotic risk profile similar to coxibs
103
Q

Current guidance on coxibs and diclofenac

A

Both C/I for ischaemic heart disease, peripheral arterial disease, cerebrovascular disease and congestive heart failure

104
Q

Why worry about 3 in 1000 thrombotic effects when using coxibs and NSAIDs?

A

Statins (at 20% 10 year CVD risk) reduce rate of events by 5 in 1000 people per year
UK pop. about 65% NSAID plus COX2 prescribing is diclofenac or coxibs
For individual trade off benefits/risks

105
Q

Paracetamol vs oral NSAID evidence summary:
Efficacy
Safety

A
  1. Paracetamol provides less pain reduction than oral NSAIDs
  2. Oral NSAIDs greater risk of GI adverse effects than paracetamol
    COX2 lower GI risk than NSAID (eliminated by low dose aspirin)
    PPI reduce GI risk in patients taking NSAIDs & COX2
    COX2 & diclofenac increase CV disease risk
106
Q

NSAID induced GI events: people at high risk have 1 or more risk factors

A
  • Using max. recommended dose of NSAID
  • 65+
  • Hx gastroduodenal ulcer, GI bleeding or gastroduodenal perforation
  • Concomitant use of meds that increase GI events (anticoagulants, aspirin, corticosteroids, SSRIs, venlafaxine or duloxetine)
  • Comorbidity (CV disease, hepatic/renal impairment, diabetes, hypertension)
  • Requirement for prolonged NSAID use (OA or rheumatoid of any age, chronic low back pain and 45+)
107
Q

Paracetamol prescribing issues

A
  • Well tolerated and rarely cause ADR when used at recommended dose
  • Best avoided in hepatic impairment or alcohol dependence (liver damage risk)
  • Pregnant/breastfeeding with OA paracetamol preferred to NSAID
  • In GI risk factor patients, use paracetamol (with or without codeine)
108
Q

NSAID prescribing issues

A
  • If taking OTC aspirin or ibuprofen and need another NSAID, problem
  • If C/I to oral NSAIDs (known allergy, severe HF, GI bleed)
  • If condition where NSAIDs cautioned (asthma, IBD, renal impairment)
  • If increased GI adverse effects - additional gastroprotection needed
  • If closer monitoring for GI, CV, renal or hepatic ADRs (elderly, comorbidities)
  • If hazardous interactions (thiazide diuretics, SSRIs, warfarin)
109
Q

NSAIDs in pregnancy/breastfeeding

A

Paracetamol analgesic, antipyretic of choice during conception but occasional single dose NSAIDs unlikely to affect chances
If NSAID needed, ibuprofen preferred before 30 weeks, NSAIDs NOT used after 30 seeks without fetal monitoring

110
Q

Codeine and paracetamol
Codeine can cause?
Advice

A
  1. Prescribe separately so individually titrated, combo products (co-codamol) not recommended
  2. GI problems (N + V, constipation) if regular use, prescribe laxative
    CNS toxicity (sedation) avoid driving & activities where drowsiness affects
  3. Driving while taking weak opioids
111
Q

PPIs and liver disease

A

PPIs undergo extensive hepatic metabolism
With liver disease, do not exceed daily doses
- Omeprazole, pantoprazole & esomeprazole 20mg
- Lansoprazole 30mg
No data on rabeprazole use in severe hepatic impairment but caution advised

Pharmacy (23 decks)

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