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Locomotor > Pain & Analgesia > Flashcards

Pain & Analgesia Flashcards

1
Q

How does pain transmission occur in the nervous system?

A

Peripheral nervous system (PNS)= nociceptors

Central nervous system (CNS)= higher centres, somatosensory cortex

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2
Q

What is the importance of pain?

A
  • Defensive function: short-term reflex motor effects, long-term prevention of damage (joint), humoral effects (increase CRH which in turn releases ACTH)
  • Problems arise if pain sensation is lost (neuropathic disease= leprosy, diabetes)- Charcot joint (disrupted architecture as patient uses already damaged joint)
  • Involves higher centres of the brain
  • Anxiety, depression, insomnia, anorexia
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3
Q

What are the classifications of pain?

A
  • Physiological= somatic (skin) or visceral nociceptors (heart, gut, internal)/ usually acute, transient, heals with time
  • Inflammatory= RA
  • Vascular= ischaemia (angina), migraine
  • Neuropathic (neurogenic)= non-nociceptive pain after nerve damage/ often chronic (phantom limb, disc pain, neuralgia, stroke, diabetes, some tumours)
  • Psychogenic= pain that occurs after (or is exacerbated by) as some underlying psychological disorder, rather than in response to immediate physical injury
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4
Q

What is acute pain?

A

Short term natural physiological defence reaction that disappears once the tissue damage resolves (cut, burn, surgery)

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5
Q

What is chronic pain?

A

Persists for weeks, months or years and is often associated with chronic disease processes that are non-malignant (arthritis), malignant (cancer) or psychogenic in nature

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6
Q

What is referred pain?

A

Pain related to one part of the body felt in another (angina- left arm, hip problems felt in knee)

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7
Q

What are the common causes of acute pain?

A
  • Somatic causes= stubbed toe, sting, cut, burn, toothache, post-operative
  • Visceral causes= appendicitis, myocardial infarction, angina pectoris, childbirth
  • Other acute pain= migraine, headaches
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8
Q

What are the common causes of chronic pain?

A
  • Musculoskeletal= back pain, osteoporosis
  • Chronic inflammation= RA, IBD
  • Neuropathic pain= diabetes
  • Cancer
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9
Q

What are the 4 stages of pain perception?

A
  1. Pain ‘sensing’ in the peripheral tissues by activation of specialised pain receptors (nociceptors)
  2. Transmission of pain information in afferent nerve fibres from the periphery to the spinal cord
  3. Transmission from the dorsal horn of the spinal cord, where it can be inhibited or amplified by local spinal circuits or descending tracts from higher brain centres, through the spinal cord to the brain
  4. Analysis of the information in higher brain centres, from where appropriate action can be initiated
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10
Q

What is each stage of pain perception influenced by?

A
  • Peripheral sites: local chemical mediators
  • Afferent nerves: local chemical mediators
  • Spinal cord: descending inhibition, neurotransmitters in spinal cord
  • Central sites: neurotransmitters
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11
Q

Why are some people more sensitive to pain than others?

A
  • Genetics (certain Na+ channels on nociceptors, opioid receptors)
  • Conditioning by experience (needle in blood tests)
  • Family attitude
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12
Q

What are Nociceptors?

A
  • Specialised nerve endings amenable to various stimuli
  • Specific to pain (not touch)
  • Two main locations
  • Somatic pain= skin, joints, cornea, tongue, teeth, joints, nipples, testicles, others, painful sensation good discrimination
  • Visceral pain= heart, gut, bile duct, ureter, poor discrimination (often diffuse or referred)
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13
Q

What chemicals are involved with nociceptors?

A
  • Nociceptors are bare nerve endings found in skin, muscle and deeper viscera
  • Directly activated by: release of chemicals (histamine, bradykinin), mechanical forces, temperature (hot and cold), tissue injury and inflammation, nerve damage (neuropathy)
  • Bradykinin is a well-known chemical that acts via G-protein-coupled receptors (B1 and B2) leading to pain, vasodilation, oedema and activation of membrane bound phospholipase A2 (inflammation)
  • Serotonin and histamine from mast cells, K+, lactic acid (ischaemia), H+ and ATP from damaged cells
  • prostaglandins increase sensitivity to pain but do not cause pain themselves
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14
Q

Describe peripheral pain fibres

A

Myelinated Adelta fibres
-Rapid transmission at 15 m/s
-Localised
-Sharp, fast, intense pain
Unmyelinated C fibres
-Slow transmission at 1 m/s
-Poorly localised
-Dull, slow, throbbing, burning, aching pain
Cell bodies are the dorsal toot ganglion
Afferent fibres synapse with nociresponsive neurones in dorsal laminae of spinal cord
These ascend the spinal cord in the contralateral spinothalamic tracts

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15
Q

What are the key excitatory neurotransmitters at the synapse between the afferent fibres and ascending nociresponsive neurones?

A
  • Amino acid: glutamate acting at AMPA and NMDA receptors
  • Neurokinins: substance P acting at neurokinin A receptors
  • Other neuropeptides include somatostatin, VIP and cholecystokinin
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16
Q

What are the key inhibitory influences on cord pain sensitivity?

A
  • Metenkephalin and beta-endorphin acting at GPCR opioid receptors which inhibit glutamate and substance P release at C fibres by blocking voltage-gated Ca2+ channels (opioid activation reduces cAMP, opens K+ channels to hyperpolarise neurons)
  • Noradrenaline and 5-ht
  • GABA and glycine
  • Modulatory activity in changing periphery nociceptor activation
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17
Q

What is spinal ‘wind-up’?

A

Chronic potentiation of the depolarisation in spinal neurones due to repetitive activation of c fibres meaning that further acute stimuli can cause prolonged response (hyperalgesia) because of priming (NMDA receptor-based response in spinal cord)

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18
Q

What is the Gate control theory of pain?

A

Peripheral pain signals have to get through the ‘gate’ at the initial synapse which may be influenced by other factors

  • The activity of neurones that transmit pain in the spinal cord can be influenced/ inhibited by other factors that may reduce transmission of impulses to the brain and these include
  • Descending nerve impulses from the thalamus and cerebral cortex, areas of the brain that regulate thoughts and emotions
  • Other local sensory inputs such as rubbing the skin around an affected area (NB the use of TENS)
  • The theory explains why thoughts and emotions modify the perception of pain and why interventions (imagery, distraction) give relief
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19
Q

Describe the transmission to the brain

A
  • Spinal cord transmission in the contralateral spinothalamic tracts
  • Higher brain centres involved in pain: thalamus, cerebral cortex (cognitive response), limbic system (emotional response)
  • Opioid receptors are found throughout the central nervous system, natural endogenous enkephalins
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20
Q

What are the CNS targets for analgesic drugs?

A
  • Spinal cord transmission: Excitatory (substance P, glutamate), inhibitory (GABA, glycine)
  • Descending pathways: inhibitory (5-HT, noradrenaline, enkephalin), excitatory descending pathways
  • Opioids can influence the mechanism at various levels
  • Target receptors= agonists to mimic endogenous analgesics, antagonists to block algogens (initiate pain), drugs to block synthesis of transmitter
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21
Q

What are analgesic drugs?

A

Drugs that relieve pain without blocking nerve impulse conduction or markedly altering sensory function
-Rule out local and general anaesthetics

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22
Q

What are the major classes of analgesic drugs?

A
  • Simple analgesics (paracetamol)
  • Opioid analgesics (morphine)
  • Non-steroidal anti-inflammatory drugs (ibuprofen)
  • Other drugs used to relieve pain: anti-epileptic drugs, nitrates, anti-migraine, local anaesthetics (chronic pain)
  • Centrally acting/ peripherally acting
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23
Q

What are the sites of action of analgesic drugs to treat pain?

A
  1. Tissue damage and local mediators that stimulate nociceptors
  2. Transmission of impulses in afferent pain fibres
  3. Spinal cord synapses and transmission
  4. Response to pain information in the higher brain centres
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24
Q

What is paracetamol?

A
  • Cyclooxygenase inhibitor
  • Prevent arachidonic acid being converted into PGs (COX)
  • Structure very similar to aspirin (NSAID) but different pharmacological effects (no anti-inflammatory effect, no peripheral NSAID adverse effects- toxicity)
  • Analgesic effect mainly central action because intrathecal administration appears to be effective in pain models
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25
Q

What is the molecular action of paracetamol?

A
  • Primary site of action is probably related to central inhibition of PG synthesis
  • May involve the production of reactive metabolites by the peroxidase function of COX-2, which could deplete glutathione, a cofactor of enzymes such as PGE synthase
  • Inhibits COX-3 (iso enzyme variant), a splice variant of COX-1, although genomic and kinetic analysis indicates that this selective interaction appears to activate descending inhibitory serotonergic pathways by increasing the bioavailability of serotonin
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26
Q

What are Opioids?

A
  • Agonists at specific GPCR opioid receptors: mu receptors (main receptor analgesic effects), delta, kappa
  • Ligands for mu opioid receptors: endogenous peptides (enkephalins, endomorphins raised at stress), full agonists (morphine, methadone, fentanyl), partial agonists (buprenorphine), antagonists (naloxone- overdose)
  • Sites of action: nociceptive nerve endings, spinal cord, thalamus, midbrain, medulla
  • Other useful actions in pain: euphoria, peace, contentment, calm
  • Desensitisation (tolerance): receptor down-regulation
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27
Q

How are opioids used in analgesia?

A
  • Opioids are agonists at 3 different receptor subtypes G protein coupled (mu= highest affinity, delta, kappa)
  • Opioid receptor structure= 7 transmembrane G protein-coupled receptors (7TM GPCR)
  • Various sites of action
  • Naloxone is an opioid antagonist= high affinity for mu receptors
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28
Q

What are the synaptic effects of opioid analgesia?

A
  • Pre-synaptic= inhibits neurotransmitter release by reducing the influx of calcium
  • Post-synaptic= inhibits post-synaptic neurotransmission by activating potassium channels leading to hyperpolarisation
29
Q

What are NSAIDS?

A
  • Non-steroidal anti-inflammatory drugs
  • Inhibit the formation of pro-inflammatory and hyperalgesic prostaglandins by the enzyme COX
  • Tissue damage leads to inflammation and membrane distortion which activate phospholipase A2 which releases arachidonic acid which is then converted by COX to PGs
  • Predominant effects of NSAIDs are anti-inflammatory and anti-pyretic with some mild analgesic effects
30
Q

What are COX-1 and COX-2?

A
  • COX-1 is a constitutive (constantly present) enzyme found widely around the body; it maintains housekeeping PGs (those that control renal blood flow, platelet activity, gastroprotection)
  • COX-2 is synthesised de novo by inflammatory cells (neutrophils) to provide PGs, which promote inflammation and repair
31
Q

Which analgesic drugs are commonly prescribed in clinical practice?

A
  • Paracetamol
  • Morphine
  • Ibuprofen
32
Q

Describe paracetamol

A
  • No other similar drugs, often combined with codeine (co-codamol) and dihydrocodeine (co-dyramol)
  • Unclear mechanism of action appears to be central and involve decreased PG formation, has analgesic and anti-pyretic effects but no anti-inflammatory activity
  • Mild to moderate pain, pyrexia
  • Oral 500mg-1g 6 hourly (max 4g per day)
  • Very few adverse effects but causes hepatoxicity in overdose (oxidising, radicals)
  • Safe when not taken in excessive dose
33
Q

Describe morphine

A
  • Other similar opioid drugs: high efficacy (diamorphine, pethidine, oxycodone, methadone), low efficacy (codeine, dihydrocodeine, tramadol)
  • Agonists at mu opioid receptors in the spinal cord and brain
  • Severe visceral pain (myocardial infarction, post-operative pain)
  • Intravenous, oral, subcutaneous, intrathecal= begin with lower doses and titrate upwards
  • Adverse effects= constipation, nausea, vomiting, respiratory/ cough depression, urinary retention, hypotension, pupillary constriction (miosis), itching, wheal formation, tolerance, dependence, withdrawal syndrome
  • Important to be aware of adverse effects and increase gradually, review the need for analgesia regularly to avoid dependence
34
Q

Describe ibuprofen

A
  • Other NSAIDs: non-selective (aspirin, naproxen, diclofenac, indomethacin), COX-2 selective (celecoxib)
  • Inhibit COX isoforms to reduce PG formation which reduces pain sensitivity and ongoing inflammation, all but aspirin bind reversibly
  • Pain related to tissue injury (trauma, bone pain), pain related to inflammation (RA, gout, dental), pyrexia
  • Oral 200-800 mg 8 hourly
  • Gastrotoxicity (NB celecoxib), renal impairment, Na+/H2O retention, hypertension, bleeding (decreased TXA2-induced platelet aggregation)
  • Depends on vulnerability of patients to adverse effects, avoid elderly unless clear indication)
35
Q

What is the therapeutic approach to clinical practice?

A
  • Make a diagnosis= influences choice of analgesia and suggests remedial approaches; NSAIDS ideal for acute inflammatory pain, opioids ideal for severe visceral pain
  • Drugs or lifestyle issues (remedial factors)
  • Analgesics= paracetamol, opioids, NSAIDs, anti-migraine drugs, drugs for neuropathy, vasoactive drugs, antidepressants
  • Non-drug approaches= TENS, acupuncture
36
Q

What are the classes of analgesics?

A
  • Simple= paracetamol
  • Opioid= codeine/dihydrocodeine (weak), morphine (strong)
  • NSAIDs= aspirin (non-selective, irreversible), ibuprofen (non-selective), celecoxib (COX-2 selective)
  • WHO Pain Ladder= analgesics to treat increasingly severe pain related to cancer
37
Q

What is neuropathic pain?

A
  • Pain as a result of damage to neural tissue
  • Phantom limb pain, compression neuropathies (direct pressure on nerve), injury (spinal cord)
  • Peripheral neuropathies (diabetes, alcoholism (vitamin deficiency), HIV infection)
  • Post-herpetic neuralgia, trigeminal neuralgia
  • Burning, shooting or scalding (sometimes very severe)
38
Q

How is neuropathic pain managed?

A
  • Tricyclic antidepressants: amitriptyline, nortriptyline (unlicensed indications)
  • Antiepileptic drugs: gabapentin
  • Opioid analgesics: tends not to respond well
  • Topical local anaesthetic preparations: lidocaine medicated plasters
  • Capsaicin: cream licensed for post-herpetic neuralgia
  • Corticosteroids: relieve pressure in compression neuropathy
  • Neuromodulation by spinal cord stimulation
  • Multidisciplinary management: physiotherapy and psychological support
39
Q

What drugs are used for neuropathic pain?

A
  • Carbamazepine
  • Sumatriptan
  • Glyceryl trinitrate
40
Q

Describe Carbamazepine

A
  • Other drugs for neuropathic pain= anti-epileptic (gabapentin, phenytoin), antidepressants (amitriptyline)
  • Blocks voltage-gated sodium ion channels in the recovery phase thereby keeping the channels closed and resistant to activation for a longer time period than usual
  • Epilepsy, neuropathic pain related to neurological damage (nerve fibres, spinal cord, CNS) from processes such as trauma, surgery, diabetic neuropathy, cancer, HIV, post-herpetic and other neuropathies (trigeminal neuralgia)
  • Oral administration (CNS depressant)
  • Drowsiness and dizziness
  • Monitor symptoms such as pain relief and adverse affects, blood levels
41
Q

Describe Sumatriptan

A
  • Other ‘triptans’= almotriptan, eletriptan, frovatriptan, naratriptan, rizatriptan, zolmitriptan
  • 5HT2 agonists that cause vasoconstriction
  • Migraine attacks: used during the established headache phase of an attack and is the preferred treatment in those who fail to respond to conventional analgesics (vasoconstriction then vasodilatation)
  • Oral, subcutaneous, intranasal
  • Tingling, heaviness, pressure, coronary vasospasm
  • Monitor impact on symptoms
42
Q

Describe Glyceryl trinitrate

A
  • Other nitrates: isosorbide mononitrate
  • Broken down in vascular tissues to release wither NO or a Nitrosothiols, vasodilation in arterial and venous system, reduces blood pressure (afterload on the heart), reduces venous return to the heart (preload), this all reduces the mismatch between blood and oxygen supply to the heart and the energy output required
  • Angina pectoris, heart failure (acute and chronic)
  • Sub-lingual or buccal (avoids first pass metabolism)
  • Headache, dizziness
  • Monitor symptoms or angina
43
Q

What are local anaesthetics?

A
  • Act by causing a reversible block to conduction along peripheral nerve fibres by blocking sodium channels
  • Vary widely in potency, toxicity, duration of action, stability, solubility in water, ability to penetrate mucous membranes
  • Topical (surface), infiltration, peripheral nerve block, intravenous regional anaesthesia (Bier’s block), plexus, epidural (extradural) block, spinal (intrathecal or subarachnoid) block
  • Postoperative pain relief reduces need for opioids
  • Lidocaine
44
Q

Describe the administration of local anaesthetics

A
  • Rate of absorption and excretion, potency, patient’s age, weight, physique, clinical conditions, vascularity of administration site, duration of administration
  • Uptake into systemic circulation determines duration of action and produces toxicity
  • Avoid accidental intravascular injection- give slowly (administer parentally only with resuscitation equipment)
  • Long-acting local anaesthetic when prolonged analgesia is required- minimise the likelihood of cumulative systemic toxicity
  • Local anaesthesia around oral cavity may impair swallowing and increases risk of aspiration
45
Q

What are the adverse effects of local anaesthetics?

A
  • Systemic absorption resulting in excessively high plasma concentrations; severe toxicity usually results from inadvertent intravascular injection or too rapid injection
  • The systemic toxicity mainly involves the CN and cardiovascular systems
  • CNS effects= feeling inebriation and light-headedness followed by sedation, numbness and paraesthesia (sensations of hot and cold, dizziness, blurred vision, nausea, vomiting, restlessness, muscle twitching, tremors, convulsions, drowsiness, respiratory failure, unconsciousness, coma
  • Cardiovascular effects= myocardial depression, hypotension, bradycardia, cardiac arrest (Lidocaine Class 1 anti arrhythmic drug)
46
Q

Describe Lidocaine

A
  • Similar drugs= prilocaine, bupivacaine, cocaine
  • Blocks sodium channels to prevent membrane depolarisation
  • Topical application to skin and mucosa, subcutaneous injection (sometimes with adrenaline), deep injection
  • Nervous system depression depression, cardiovascular system depression
  • Care must be taken to spot signs of inadvertent systemic absorption
47
Q

Why are local anaesthetics taken with adrenaline?

A
  • Local anaesthetics cause dilation of blood vessels increasing local blood flow and the rate of absorption i.e. shortening the anaesthetic effect and increasing systemic exposure
  • Overcome by the addition of a vasoconstrictor such as adrenaline to the preparation- activates alpha-1 adrenoreceptors (vasoconstriction)
  • Avoid inadvertent intravenous administration/ in digits or appendages because of the risk of ischaemic necrosis
48
Q

What is inflammation?

A
  • Response to tissue injury that result from trauma, injection or toxicity
  • Natural/ physiological response to inevitable experience of living
  • Enable tissues to mount a defensive reaction that will enable the threat to be removed and healing occur
  • Outcome= healing/ scarring/ chronic (RA, IBD, asthma, atopic eczema)
49
Q

What are the clinical features of inflammation?

A
  • Pain= release of inflammatory mediators such as bradykinin, histamine and prostaglandins(increase sensitivity to mediators) in the vicinity of nociceptive neurones
  • Redness= vasodilation in response to these mediators increasing blood supply and initiating the repair process
  • Heat= vasodilation increases blood supply, often to colder periphery, coupled with increased local metabolic rate
  • Swelling= mediators increase the ‘leakiness’ of blood vessels allowing proteins to extravasate into the damaged area increasing the oncotic pressure which attracts fluid
50
Q

What are the inflammatory mediators from mast cell products?

A

-histamine (nociception, vasodilation, increased permeability via H2-receptor), 5-HT/ serotonin (nociception, vasoconstriction, activates collagenase 2)

51
Q

What are the inflammatory mediators that are 5-lipoxygenase products?

A

Leukotrienes (B,C,D4)= nociception, increased permeability, adhesion molecules, chemotaxis

52
Q

What are the inflammatory mediators that are cyclooxygenase products?

A

Prostaglandins (D2, E2, I2)= sensitise nociceptors, vasodilation, increased permeability (COX product)

53
Q

What are the inflammatory mediators that are macrophage products?

A
  • TNFa: fatigue, activates GM-CSF- bone erosion, cartilage destruction
  • Interleukins: IL-6, IL-8- activate B cells via specific receptors
54
Q

What are the inflammatory mediators that are enzymes?

A

-Tryptase= breaks down collagen
-Chymase= breaks down proteoglycans
Destructive in chronic

55
Q

What are the inflammatory mediators that are T-cells?

A

Interferons: activate immune cells (natural killer cells, macrophages)

56
Q

What are the inflammatory mediators in blood?

A

Fibrin, antibodies, complement, C-reactive protein, PMNs

57
Q

What are the drugs used to treat inflammation?

A
  • Non-steroidal anti-inflammatory drugs= aspirin, ibuprofen, diclofenac, indomethacin
  • Corticosteroids= hydrocortisone, prednisolone, dexamethasone
  • Other: disease-modifying anti-rheumatic drugs (DMARDs), immunosuppressive drugs
58
Q

What are NSAIDs in inflammation?

A
  • Most developed several years after corticosteroids
  • Principle mechanism of action is inhibition of the enzyme COX
  • Pharmacological effects= analgesic, antipyretic, anti-inflammatory (higher doses)
  • Adverse effects
  • Salicylates (diflunisal), propionic acid derivatives (ibuprofen, naproxen), acetic acid derivatives (indomethacin), fenamic acid derivatives (mefenamic acid), coxibs (celecoxib)
59
Q

What are the adverse effects of NSAIDs?

A
  • Risk factors= chronic use, older patients, higher doses, differ between drugs
  • Gastrotoxicity, nephrotoxicity, cardiovascular
60
Q

What are coxibs?

A
  • Selective cyclo-oxygenase-2 (COX-2) inhibitors

- arachidonic acid= COX-1 (PGs, TXA2, gastric cytoprotection, platelet aggregation) COX-2 (PGs, inflammation, pain)

61
Q

What are corticosteroid drugs?

A
  • Analogues of the endogenous glucocorticoid hormones that are synthesised and released by the adrenal cortex in response to ACTH in pituitary gland
  • Dramatic response of previously untreatable conditions like RA, SLE and asthma
  • Within a few years it became clear that the long-term adverse effects would make chronic systemic corticosteroid therapy impossible
62
Q

What are the actions of corticosteroids?

A

Hypothalamus (CRF- corticotrophin releasing factor) Pituitary gland (ACTH- corticotrophin) Adrenal gland- glucocorticoid + receptor= RNA to mRNA to protein synthesis to steroid response
Negative feedback mechanism on hypothalamus so exogenous supply inhibits natural supply

63
Q

What are the pharmacological effects of corticosteroids?

A
  • Inflammatory responses decrease
  • Immunological responses decrease
  • Glycogen synthesis (liver) increase
  • Gluconeogenesis increase
  • Glucose output (liver) increase
  • Glucose utilisation decrease
  • Protein catabolism increase
  • Bone catabolism increase
  • Mood increase
  • Gastric acid and pepsin increase
  • Na+ reabsorption increase
  • K+/H+ excretion
64
Q

Describe prednisolone

A
  • Other corticosteroid: oral (hydrocortisone), IV/M (hydrocortisone, methylprednisolone, dexamethasone), inhaled (beclomethasone), topical (hydrocortisone, betamethasone)
  • Bind to intracellular receptors to alter translation of DNA, macrophages and T cells are key cell targets in inflammation
  • Inflammatory disease such as asthma, COPD exacerbations, RA, SLE, IBD, allergic emergencies
  • Oral 10-40 mg tds
  • Skin changes, osteoporosis, myopathy, diabetes, hypertension, growth suppression, infection
  • Required monitoring for long-term use, lowest dose for shortest time period
65
Q

What are the important adverse effects of corticosteroids?

A
  • Adrenal suppression
  • Susceptibility to infections
  • Diabetes
  • Muscle wasting
  • Growth suppression
  • Osteoporosis
  • Psychosis
  • Peptic ulceration
  • Na+, H2O retention, hypokalaemia, hypertension, muscle weakness
66
Q

What are other drugs to treat inflammation?

A
  • DMARDs= sulfasalazine, methotrexate, infliximab

- Immunosuppressive drugs= azathioprine, cyclophosphamide, cyclosporine

67
Q

What are the effects of thromboxane?

A

TXA2
Platelet aggregation
Vasoconstriction

68
Q

What are the effects of prostacyclin?

A

PG12
Vasodilation
GI mucosal protection

69
Q

What are the effects of prostaglandins?

A

PGE1, 2
Kidney vasodilatation
GI tract protection
CNS

Locomotor (20 decks)

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