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Title: Clinical%20Pharmacology


1
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2
  • Clinical Pharmacology
  • of Analgesic Medications
  • Non-Phramacologcial Treatments
  • type in your name

type in the name of your institution
3
Contents of this Lecture
  • (1) Clinical Pharmacology of
  • Paracetamol (Acetaminophen)
  • Non-steroidal anti-inflammatory drugs (NSAIDS) /
    COX-2 specific inhibitors
  • Opioids
  • Ketamine
  • Drugs used for neuropathic pain
  • Local Anaesthetic agents
  • Others - Steroids
  • (2) Non-drug treatments

4
Clinical Pharmacology includes
  • Mechanism of Action
  • Absorption / Elimination of the drug
  • Indication for use / dosage
  • Adverse / side effects
  • Any special precautions that should be taken

5
Paracetamol
  • Paracetamol has been in use for more than a
    century
  • It has both analgesic and antipyretic action
  • However, the exact mechanism of its action is
    unclear
  • Absorption / Elimination from the body
  • It is well tolerated when taken orally.
  • On oral administration it is absorbed from the
    intestine (70), stomach and colon (30)
  • The rate of absorption is rapid and depends on
    the dose

6
Absorption / Elimination
  • The time taken to reach maximum plasma
    concentration (Tmax) is 15 - 30 minutes depends
    on the preparation
  • It is available as tablets (adults), suspension
    or syrup for children and suppositories
  • Tmax is 2 - 3 hours with suppositories
  • Bioavailability ranges from 60-90
  • Elimination
  • Paracetamol is metabolized in the liver and only
    2 - 5 is excreted unchanged

7
Indications and dosages
  • It is used as an analgesic drug for mild to
    moderate pain
  • E.g. Tooth ache / teething pain in children,
    backpain, joint and muscle pain, headache,
    dysmenorrhoea
  • Relief of fever in adults and children
  • Dosage
  • Adults Up to 1g oral / rectal, every 6 hours (
    4g should not be exceeded / day
  • Children Oral / rectal 20 mg / kg every 6
    hours

8
Side effects
  • Paracetamol is well tolerated and has no side
    effects at therapeutic doses
  • It has good haematological tolerability and does
    not alter haemostasis

9
Caution
  • Since it is metabolized in the liver it must be
    used with caution / or omitted in the presence of
    liver impairment
  • In patients with renal impairment, the dose of
    paracetamol should be reduced
  • Do not exceed 4g/day in adults and 125 mg/ kg in
    children

10
Adverse effects
  • Hepatotoxicity with an overdose of paracetamol
  • This can occur when a patient does not get
    adequate relief with paracetamol and decides to
    take more than the prescribed dose of a maximum
    of 4g/day (8 - 10 g / day)
  • Intentional overdose (Paracetamol overdose /
    poisoning is the leading cause of acute liver
    failure in the US, UK and Australia)
  • Overdose causes acute liver failure, as the
    elimination pathways are saturated resulting in
    elevated levels of toxic metabolites

11
Adverse Effects
  • N-acetylcysteine (NAC) is the antidote for
    paracetamol poisoning and it is most effective
    when administered within 8 - 10 hours after
    ingestion
  • Renal toxicity Overdose can cause severe
    kidney necrosis
  • Allergic reactions are rare

12
NSAIDs
  • Non Steroidal Anti-inflammatory Drugs

13
History of Aspirin
  • Salicylate from the bark of the willow tree and
    was used to treat fever and rheumatism for
    centuries
  • In the late 19th century, salicylic acid and
    later acetylsalicylic acid was synthesized and
    called aspirin.
  • Aspirin was widely used to treat fever and pain
    till the availability of other drugs with similar
    mechanisms of action. It continues to be used in
    many parts of the world

14
Non-Steroidal Anti-inflammatory Drugs (NSAIDs)
  • They are diverse group of compounds which were
    later synthesized, with actions similar to that
    of aspirin and became known as NSAIDs
  • The mechanism of action of aspirin / NSAIDs was
    discovered in the 1960s by Prof Vane, who was
    awarded a Nobel prize in Medicine in 1982

15
Non-steroidal Anti-inflammatory Drugs -NSAIDs
  • NSAIDs are widely used to treat pain and
    inflammation
  • They act through inhibition of the two isoforms
    of the enzyme cyclooxygenase (COX) i.e. COX-1
    and COX-2
  • NSAIDs that act on both the enzymes are known as
    non-selective NSAIDs (ns-NSAIDs)
  • NSAIDs which act predominantly on the COX-2
    enzyme are known as specific COX-2 inhibitors
    (also referred to as Coxibs)

16
The Two Isoforms of COX
  • COX-1 is a normal constituent in the body for
    homeostasis, such as in
  • Gastric mucosa gastric cytoprotection
  • Kidney Sodium and water balance / renal
    perfusion
  • Platelets for aggregation
  • COX-2 is induced in the presence of injury and
    inflammation
  • COX-2 is also a normal constituent in the many
    organs such as Kidney, brain, endothelium, ovary
    and uterus

17
What happens when there is tissue injury?
Cell wall injury
Releases
Membrane phospholipids
Phospholipase A2
Arachidonic Acid
COX-1 COX-2 that is induced with injury and
inflammation, cancer
PGH2
(Prostaglandin H2)
PGD2
TXA2
PGE2
PGI2
PGF2
Prostaglandins- PGE2 as the most significant
Thromboxane
18
Arachidonic Acid Cascade
Phospholipid from cell membrane
Arachidonic Acid
Lipoxygenase
Cyclo-oxygenase
PGH2
5-HPETE
Leukotrienes
Prostaglandins
Thromboxane
These inflammatory mediators activate the
nociceptors on the Ad and c fibres and result in
pain and sensitization
19
Arachidonic Acid Cascade
Phospholipid from cell membrane
Arachidonic Acid
NSAIDs / COX-2 inhibitors
Lipoxygenase
Cyclo-oxygenase
PGH2
5-HPETE
Leukotrienes
Prostaglandins
Thromboxane
Reduce Prostaglandins and Thromboxane, resulting
in reduced pain
20
ns-NSAIDs
COX-2 specific inhibitors ( Coxibs)
  • Acetylsalicylic acid (aspirin)
  • Tablet, suppository
  • Ibuprofen
  • Tablet, suspension for children
  • Indomethacin
  • Tablet
  • Diclofenac
  • Oral tablet, suppositories, parenteral form
    available
  • Mefenamic acid
  • Oral tablets
  • Celecoxib
  • Oral capsules
  • Etoricoxib
  • Oral tablets
  • Parecoxib
  • parenteral

21
Anti-Pyretics / NSAIDs on the WHO essential drug
list
  • Acetylsalicylic acid (Aspirin)
  • Tablet 100 mg to 500 mg
  • Suppository 50 mg to 150 mg
  • Ibuprofen gt 3 months in age
  • Tablet 200 mg 400 mg
  • Oral liquid 200 mg / 5 ml
  • Paracetamol
  • Tablet 100 mg to 500 mg
  • Suppository 100mg, 250 mg
  • Oral Liquid 125 mg / 5 ml

22
Absorption and Elimination
  • When administered orally, aspirin, ns-NSAIDs and
    Coxibs are well absorbed and reach therapeutic
    levels within 30 to 60 minutes.

23
Indications
  • Both the ns-NSAIDs and Coxibs have the same
    efficacy in postoperative analgesia
  • Sole analgesia for day surgery
  • Along with opioids for major surgery
  • Musculo-skeletal pain e.g. back pain, joints,
    muscle sprains etc.
  • Osteoarthritis
  • Rheumatoid arthritis
  • Not indicated for neuropathic pain

24
Side effects / Adverse effects
  • Gastrointestinal effects
  • The risk of erosions, ulcers and bleeding is
    higher with ns-NSAIDs compared to Coxibs.
  • This risk with ns-NSAIDs is also variable with
    some being less than others.
  • Risk is greater
  • In elderly patients
  • Those who are also taking aspirin
  • Risk can be reduced by adding a proton-pump
    inhibitor (e.g. omeprazole) to ns-NSAIDs.
  • H2 receptor blockers are not very effective.

25
Renal effects
  • Both COX-1 2 are constituent enzymes in the
    kidney
  • Maintain renal perfusion and sodium/water balance
  • Both ns-NSAIDs and Coxibs can cause
  • Hypertension, odema
  • Decrease in creatinine clearance that may be
    significant in patients with impaired renal
    function or transient hypotension / hypovolaemia
    in the postoperative period

26
Cardiovascular effects
  • Some studies have shown that there was a higher
    risk of thrombotic cardiovascular events
    (stroke, heart attack) when on Coxibs when
    compared to ns-NSAIDs such as naproxen
  • Other studies have shown that the cardiovascular
    events are similar
  • Nevertheless, current recommendations are that
    Coxibs should not be used in patients with active
    cardiovascular disease and a known thrombotic
    condition

27
Effect on platelets
  • ns-NSAIDs are able to prevent platelet
    aggregation as platelets do not have COX-2. There
    is therefore a potential for bleeding with
    ns-NSAIDs
  • Coxibs do not prevent platelet aggregation
  • ns-NSAIDs should be used with caution in patients
    who are already on aspirin

28
Others
  • Some ns-NSAIDs can precipitate asthma is aspirin
    sensitive asthmatic patients.
  • Coxibs are well tolerated by patients who have
    aspirin sensitive asthma

29
Summary (cont.)
  • NS-NSAIDs / Coxibs
  • Both drugs are effective in providing pain relief
    for moderate pain
  • The mechanism of action of both groups of drugs
    is by inhibiting the COX-2 enzyme that is induced
    with injury, inflammation and cancer
  • Gastrointestinal side effects are less with
    coxibs

30
Summary
  • NS-NSAIDs / Coxibs
  • Coxibs have no effect on platelet aggregation
  • Both drugs should be used with caution in
    patients with renal impairment and in the elderly
  • Coxibs should not be used in patients with active
    cardiovascular disease or known thrombotic
    effects
  • Coxibs can be given to patients with aspirin
    sensitive asthma
  • Both drugs should be used for the shortest period
    of time at the lowest dosage

31
Opioids
32
Opioids
  • Opium alkaloids derived from the opium poppy has
    been used for pain relief for centuries
  • Morphine was isolated by Sertuner in 1813
  • The glass syringe was introduced in 1844
  • Since then morphine has been the mainstay in the
    management of severe pain
  • The term opioid is referred to any drug, either
    natural, semi-synthetic or fully synthetic, which
    has actions similar to morphine

33
Available Opioids
  • Natural
  • Morphine
  • Codeine
  • Semi-Synthetic
  • Hydromorphone
  • Oxycodone
  • Diacetylmorphine(heroin)
  • Naloxone (antagonist)
  • Fully Synthetic
  • Pethidine (meperidine)
  • Tramadol
  • Nalbuphine
  • Methadone
  • Pentazocine
  • Fentanyl
  • Alfentanil
  • Sufentanil
  • Remifentanil
  • Opioids on the WHO essential drug list
  • Morphine
  • Codeine
  • Tramadol

34
Opioids can be classified as
  • Strong opioids used for severe pain
  • Morphine, Oxycodone, Pethidine, Fentanyl
  • Weak Opioids used for moderate pain
  • Codeine, Tramadol

35
The analgesic ladder for acute pain management
Strong opioids
Weak opioids
36
Mechanism of Action
  • Opioids act by binding to opioid receptors
    (complex proteins embedded within the cell
    membrane of neurons)

There are three different opioid receptors - µ,
d, ? µ - most relevant as all clinically used
opioids exert their action via the µ -opioid
receptor
Opioid receptors are found in the brain and in
the dorsal horn of the spinal cord
37
Mechanism of Action
  • Opioids bind to opioid receptors
  • Activate intracellular signaling events
  • Leading to reduction in excitability of neurons
    and inhibition of pain signals
  • Resulting in reduction of pain perception

38
Opioids can be administered via several routes
  • Opioids produce potent analgesia when
    administered
  • Systemically oral, Intravenous, intramuscular,
    subcutaneous, transcutaneous, per rectal
  • Spinally epidural, intrathecal,
    intraventricular
  • Time to peak action and duration of action
    depends on the route and dose of the drug

39
Morphine
  • Is the most widely used opioid for the control
    of severe pain
  • It can be given by all the routes that was
    described in the previous slide.
  • It is well absorbed when given orally and has a
    bio-availability of around 30-35.
  • Bio-availability means the amount of drug that is
    available in the systemic circulation after an
    oral dose is given.

40
Oral morphine
  • Immediate release morphine
  • Aqueous / liquid morphine (usually prepared as
    1-2 mg / ml)
  • Tablet morphine (10 mg)
  • Need to be given every four hours for continuous
    relief of severe pain
  • Sustained Release (SR) Morphine Tablets
  • Morphine is released slowly over 12 hours
  • 10 mg, 30 mg, 60 mg
  • These tablets are given twice a day

41
Parenteral morphine (10 mg / I ml ampoule)
  • Intramuscular / subcutaneous morphine
  • Onset of Analgesia 15 - 20 min
  • Peak action 45 - 90 min
  • Duration of action 4 hours
  • Intravenous route is chosen when rapid control of
    severe pain is desired.

42
Metabolism
  • The principle pathway of metabolism is
    conjugation with glucuronic acid in hepatic and
    extra-hepatic (kidney) sites
  • Morphine -3 and morphine -6 glucuronides that are
    excreted mainly by the kidneys
  • Morphine should be used with caution in patients
    with hepatic and renal impairment

43
Codeine phosphate Weak opioid
  • Oral tablet 15mg 30 mg
  • Is well absorbed and there is no first pass
    metabolism in the liver
  • Codeine is metabolized to morphine which
    accounts for its analgesic effect
  • 60 mg of codeine has an equi-analgesic effect of
    650 mg aspirin
  • Has an anti-tussive effect and is often used in
    cough mixtures
  • Is available in combination with paracetamol
  • Cause minimal sedation, nausea, vomiting and
    constipation

44
Tramadol Weak opioid
  • This is also known as an atypical opioid
  • It has a dual mechanism of action
  • weak opioid receptor binding properties
  • Inhibits the reuptake of serotonin and
    noradrenaline at the descending inhibitory
    pathway
  • It is available
  • Oral capsule (50 mg)
  • Injection 50 mg / ml in 2 ml ampoules
  • Due to its weak opioid activity it is not placed
    in the same schedule as the strong opioids such
    as morphine

45
Tramadol
  • It is well absorbed when given orally
  • Time to effect is around 30 minutes and can last
    5 - 6 hours
  • Sedation is minimal
  • Can cause nausea, vomiting, dizziness
  • Abuse potential is minimal
  • Is used as a weak opioid, however as it has a
    dual mechanism of action its analgesic efficacy
    is superior to codeine Maximum daily dose is
    400 mg

46
Metabolism
  • Tramadol is metabolized by the liver and excreted
    by the kidneys
  • Tramadol has an active metabolite
    (O-desmethyltramadol) that is also excreted
    by the kidney
  • The daily dose should be reduced in the presence
    of chronic renal failure

47
Opioid related side effects
  • Gastrointestinal
  • Nausea and vomiting
  • Constipation
  • Sedation
  • Respiratory depression in overdose
  • Pruritus
  • Cough suppression (anti-tussive)

48
Opioid related side effects
  • On initiation of opioid therapy, patients
    frequently report acute side effects of sedation,
    dizziness, nausea and vomiting
  • After a few days these symptoms subside except
    for constipation
  • This is noted in patients with cancer pain

49
Opioids and Tolerance
  • Patients can develop tolerance when opioids are
    used for an extended period
  • E.g. cancer pain intensive care units
  • Tolerance is defined as reduction of the
    pharmacological effect of an opioid
  • When the same dose produces a lesser effect
  • Increasing doses of drug is required to produce
    the same effect
  • The mechanisms of the development of tolerance
    are complex

50
Physical Dependence and Addiction
  • Physical dependence is a state of adaptation by
    the body with extended use of an opioid
  • It is manifested by withdrawal symptoms with
    abrupt cessation of the opioid, rapid dose
    reduction or administration of an opioid
    antagonist
  • Addiction to opioids is drug seeking behaviour
    where the person is looking for opioids for its
    euphoric action rather than pain relief alone

51
Ketamine is on the WHO essential drug list
  • It is a phencyclidine derivative
  • It has been used to provide anaesthesia for many
    years
  • The side effect of hallucinations has limited its
    use as an anaesthetic agent
  • Ketamine causes an increase in blood pressure and
    heart rate, hence it is used as an induction
    agent when a patient is in shock
  • It has multiple mechanisms of action
  • The main mechanism of action is that of a
    non-competitive antagonist at the NMDA receptors

52
Ketamine
  • Routes of administration
  • Intravenous
  • Intramuscular / Subcutaneous (onset 10 - 15
    min)
  • Oral (bioavailability 20) / sublingual (30) /
    rectal (30)
  • Metabolized by the liver
  • Metabolites are about 1/5th as potent as ketamine

53
Ketamine has potent analgesic properties
  • Analgesia
  • Low dose ketamine 0.1 - 0.5 mg / kg / hr can
    provide excellent analgesia
  • It can reduce opioid requirements in the
    postoperative period
  • It can be used for the management of neuropathic
    pain such as in patients with complex regional
    pain syndrome
  • As an adjunct for the relief of cancer pain,
    particularly for the neuropathic component

54
Ketamine
  • 5mg / kg IM can be used for painful dressing
    change in children
  • An anti-sialagogue should be added as it causes
    salivary secretions that can cause coughing /
    laryngospasm

55
Side effects of ketamine
  • Dizziness
  • Hallucinations
  • Emergence delirium when larger doses are used
  • Benzodiazepines can reduce these side effects
  • Salivary secretions
  • Anti-sialagogues should be used with ketamine

56
Ketamine and drug abuse
  • In recent years, ketamine has been known to be
    abused for its euphoric effects
  • Long term use can lead to cognitive impairment
    and memory loss

57
Drugs for Neuropathic Pain
58
Neuropathic pain
  • Is defined as pain that arises as a result of
    injury or disease of the somatosensory system
  • Neuropathic pain is not responsive to ns-NSAIDs.
  • Poorly responsive to Opioids

59
Drugs used for treating neuropathic pain
  • Amitriptyline
  • Carbamazepine
  • Sodium valproate
  • Gabapentinoids (not on the WHO essential drug
    list)

60
Amitriptyline
  • Is a tri-cyclic anti-depressant drug
  • Used more for the management of neuropathic pain
    than for symptoms of depression
  • Low dose amitryptyline is a first line drug for
    neuropathic pain
  • Mechanism of action
  • Inhibits the reuptake of noradrenaline and
    serotonin (thus increasing these two
    neurotransmitters) at the descending inhibitory
    pathway
  • The descending inhibitory tract influences the
    output of the neurons in the dorsal horn of the
    spinal cord

61
Absorption / Elimination
  • Amitriptyline is well absorbed on oral
    administration
  • Bioavailability 30 - 60
  • Effects last 2 - 12 hours
  • Metabolized in the liver (de-methylation) and
    excreted in the urine

62
Adverse effects
  • Common ones
  • Dry mouth, disturbances of visual accommodation
  • Constipation and urinary retention
  • Light-headedness, drowsiness
  • Less common effects
  • Cardiac Arrhythmias
  • It should be used cautiously in the elderly and
    in those with a history of cardiovascular disease

63
Carbamazepine
  • Is an antiepileptic drug
  • It is currently the drug of choice for the
    management of pain in patients with trigeminal
    neuralgia
  • Mechanism of action
  • It blocks the frequency and use of the
    voltage-gated neuronal sodium channels
  • Limits repetitive firing action of action
    potentials
  • There is a proliferation of sodium channels when
    there is nerve injury thus the efficacy of
    carbamazepine in patients with neuropathic pain

64
Side effects
  • The most common side effects are neurotoxic and
    dose-related. They include
  • Drowsiness, diplopia, headache, ataxia, nausea
  • Vomiting, dizziness
  • These side effects tend to occur within a week of
    initiation or dosage increase.
  • In chronic therapy, they typically are noticeable
    3 - 4 hours after a dose (associated with peak
    serum concentrations)
  • Systemic effects
  • Abdominal pain, diarrhea, hyponatraemia in the
    elderly

65
Serious side effects
  • Agranulocytosis and aplastic anaemia
  • Skin eruptions and life threatening
    Steven-Johnsons syndrome
  • Blood tests should be done early in the course of
    therapy and patients should be asked to report
    easy bruising.

66
Interaction with other drugs
  • Carbamazepine is an inducer of CYP450 in the
    liver
  • Efficacy of other drugs are reduced notably e.g.
  • Warfarin
  • Phenytoin
  • Valproic acid
  • Some drugs reduce the metabolism of carbamazepine
    and therefore increase its plasma level
  • Erythromycin
  • Cimetidine
  • Calcium channel blockers

67
Local Anaesthetics (LA)
  • Lignocaine (short acting) 0.5, 1.0, 2.0
    solutions
  • Bupivacaine (long acting) 0.5
  • Both belong to the amide group of LA drugs
  • Mechanism of action
  • LA drugs act by producing a reversible block to
    the transmission of peripheral nerve impulses
  • i.e. they block membrane depolarization of all
    excitable tissue, in particular the nerves
  • This action is on the sodium channels of the
    peripheral nerves.

68
LA drugs
  • Can provide both surgical anaesthesia and
    analgesia
  • Depends on the site of administration
  • Concentration of the drug used
  • Common routes of administration
  • Local infiltration
  • Individual nerve block
  • Plexus block
  • Epidural administration

69
Absorption / Elimination
  • LA drugs are absorbed into the systemic
    circulation from the site of administration
  • Rate of absorption depends on the site
  • Addition of adrenaline can delay absorption
  • After absorption, they are distributed rapidly
    and taken up by organs
  • Metabolized in the liver and excreted by the
    kidney
  • LA cross the placenta, but their effects are of
    minimal significance

70
Systemic toxicity
  • If significant amounts of LA drugs are absorbed
    they can cause toxicity
  • Nervous system
  • Numbness and tingling over the circumoral area
  • Anxiety, Light-headedness, tinnitus
  • Loss of consciousness and convulsions
  • Heart
  • Direct myocardial depression and hypotension
  • Vasodilatation
  • Cardiac arrest

71
Systemic toxicity can occur due to
  • Inadvertent intravenous administration of LA
    drugs
  • Overdose if the following limits are exceeded
  • Lignocaine plain 4 mg / kg
  • Lignocaine with adrenaline 7 mg / kg
  • Bupivacaine 2 mg / kg

72
Other Drugs (Miscellaneous category)
  • Steroids
  • Dexamethasone , Prednisone

73
Dexamethasone
  • Is a potent synthetic member of the
    glucocorticoid class of steroid drugs
  • It acts as anti-inflammatory
  • Immunosuppresant
  • Can be taken orally and is more potent than the
    naturally occurring hormone cortisol
  • Used to reduce pain and inflammation in
  • Rheumatoid arthritis

74
Non-pharmacological treatments
  • Both physical and psychological factors affect
    our perception of pain. Treatments include
  • Physical
  • Rest, Ice (cold), Compression, Elevation of
    injuries
  • Surgery (e.g. draining an abscess / fixing
    fractures)
  • Acupuncture, massage, physiotherapy
  • Ultrasound therapy
  • Transcutaneous electrical nerve stimulation
    (TENS)

75
Psychological treatments
  • Adequate explanation
  • Reassurance that their pain will be addressed
  • Counseling
  • Individual
  • Family
  • This is particularly important when dealing with
    patients with cancer pain
  • Cognitive Behavioural Therapy (CBT) for chronic
    non-cancer pain

76
Conclusion Adequate control of pain requires
  • An understanding the mechanisms of pain
  • Nociceptive or neuropathic pain
  • An understanding of the drugs that help to
    control it
  • Mechanism of action
  • Pharmacokinetics (Absorption and time to onset
    and peak action and elimination)
  • Side effect profile

77
This talk was originally prepared by
  • Ramani Vijayan, M.D.
  • Kuala Lumpur, Malaysia

78
International Pain School
Talks in the International Pain School include
the following
Physiology and pathophysiology of pain Nilesh Patel, PhD, Kenya
Assessment of pain taking a pain history Yohannes Woubished, M.D, Addis Ababa, Ethiopia
Clinical pharmacology of analgesics and non-pharmacological treatments Ramani Vijayan, M.D. Kuala Lumpur, Malaysia
Postoperative low technology treatment methods Dominique Fletcher, M.D, Garches Xavier Lassalle, RN, MSF, Paris, France
Postoperative high treatment technology methods Narinder Rawal, M.D. PhD, FRCA(Hon), Orebro, Sweden
Cancer pain low technology treatment methods Barbara Kleinmann, MD, Freiburg, Germany
Cancer pain high technology treatment methods Jamie Laubisch MD, Justin Baker MD, Doralina Anghelescu MD, Memphis, USA
Palliative Care Jamie Laubisch MD, Justin Baker MD, Memphis, USA
Neuropathic pain - low technology treatment methods Maija Haanpää, MD, Helsinki Aki Hietaharju, Tampere, Finland
Neuropathic pain high technology treatment methods Maija Haanpää, M.D., Helsinki Aki Hietaharju, M.D., Tampere, Finland
Psychological aspects of managing pain Etleva Gjoni, Germany
Special Management Challenges Debra Gordon, RN, DNP, FAAN, Seattle, USA
79
International Pain School
The project is supported by these organizations
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