Please enable JavaScript.
Coggle requires JavaScript to display documents.
Pain Syndromes and Migraine - Coggle Diagram
Pain Syndromes and Migraine
Pain
Definition
An unpleasant sensory and emtional experience associated with actual or potential tissue damage, or described in terms of such damage
Pain pathway
Peripheral nerve
Spinal cord
Cerebral cortex
Triggers
Noxious stimulus
Lesions in the peripheral / central nervous system
Classification
Aetiology
Nociceptive
Perception of pain due to tissue damage
Somatic
Skin lesions
Teeth
Pleura
MSK
Bonepain
Arthritis
Visceral
Heart
Gut
Bladder
Neuropathic
Pain initiated or caused by a primary lesion / dysfunction in nervous system
Peripheral
Diabetic peripheral neuropathy
Postherapetic neuralgia
Central
Post stroke
Post MI
Duration
Acute Pain
Normal, predicted, physiological repsonse to an adverse chemical, thermal or mechanical stimulus
Management
Id cause and treat
Assess severity
Non pharmacological treatment
+/- ice packs
Heat
Physio
Splinting / POP
Debridement
Analgesics
Chronic Pain
Continous or intermittent pain or discomfort which has persisted for => 3mth and for which painkillers have been taken and treatment sought recently and frequently
May be due to sensitisation, demyelination of nerves involved
Severity
Mild
Moderate
Severe
Pharmacological Management
Analgesics
Peripheral
NSAIDs
Centrally Acting
Opiods
Adjuvant drugs
WHO Analgesic Ladder
Paracetamol (Acetaminophen)
MOA
Antipyretics
Reduces fever by inhibition of prostaglandin synthesis
Analgesic
Inhibition of prostaglandin synthesis in CNS
Reduced pain perception
Dosage
Maximum
4 grams/day
PO
Adverse Effects
Liver Toxicity
Overdose leads to
hepatic necrosis
and
liver failure
Risk factors
Hepatocellular insufficiency
Chronic alcohol abuse
Malnutrition
Dehydration
Body weight <50kg
Interactions
Warfarin
Monitor
INR
Increased anticoagulant effect and increased risk of bleeding
Anti-epiletics
Phenytoin
Carbamazepine
Phenobarbital
↑ Metabolism ↓ efficacy
Precautions
Pt w/ Liver impairment
Indications
Mild-Moderate pain
Headache
MSK pain
Post-op
Fever reduction
Chronic pain management co-perscription
NSAIDs
MOA
Analgesic and anti-inflammatory
Inhibition of prostaglandin synthesis by inhibition of COX enzymes
Selective COX-2 inhibition ass with less GI intolerance
Indications
Continous or regular pain associated with inflammation
MSK
Osteoarthritis
Lower back pain
Combined with opiods to reduce opiod dose
Administration
PO
Parenteral
Rectal
Topical
Examples
Ibuprofen
Naproxen
Diclofenac
Mefenamic acid
Prioxicam
Etoricoxib
Celecoxib
Adverse Effects
↑ Risk of GI toxicity
Peptic ulceration
Na+ and water retention
Cardiac impairment
Thrombotic events
Hypersensitivity reactions
Hepatic damage
GI haemorrhage
Contraindications / Cautions
Risk factors
Elderly
Smoking
Hx of peptic ulcers
Medications
High dosage + long duration
Elderly
Inappropriate w/ certain conditions / meds
Ischaemic heart disease
COX-2 inCardiovascular disease
Peripheral arterial disease
Heart failure
Anticoagulants
Antiplatelets without PPI prophylaxis
Hx of peptic ulcer
Hx of GI bleeding
Corticosteroids without PPI prophylaxis
eGFR <
50
mL/min/1.73m2
Severe hypertension
Opioids
MOA
Bind to μ opioid receptors, prevent Ca2+ influx and neurotransmitter release, and inhibit ascending transmission of nociceptive stimuli
Drugs
Morphine
Indications
Severe acute pain
Palliative care
Admin
Oral where possible
Codeine
MOA
Weak opioid than binds μ receptors
Pharmacokinetics
Liver
Converted to morphine
Indications
Effective mild - molderate pain when other analgesics fail
Dihydrocodeine
MOA
Semisynthetic weak opioid
Can cause histamine relase
Indications
Moderate - acute chronic pain
Tramadol
MOA
Synthetic codeine analogue - moderately potent
Opioid analgesic
Enhancement of serotonergic and adrenergic pathways
Indications
Severe pain in adults
Adverse Effects
Hypotension
Hypertension
Psychiatric reactions
Serotonin syndrome
May exacerbate seizures
Contraindications
Uncontrolled epilepsy
Hepatic and renal impairement
MOAI co-admin
Oxycodone
MOA
Powerful μ receptor agonist
Twice as potent as oral morphine
Indications
Used in morphine not tolerated / effective
Tapentadol
MOA
Strong opiod, 1/2 poten as mophine
Opioid analgesia
Inhibition of noradrenaline reuptake
Adverse Effects
Seizures
Increased risk with medication that lowers seizure threshold (SSRIs, SNRIs, TCI,)
Indications
Less vomiting, nausea, constipation as other opioids
Hydromorphone
7.5x as potent as morphine
Pethidine
Methadone
Buprenorphine
MOA
Agonist and antagonist properties
25-50x more potent than morphine
Adverse Effects
May antagonise analgesic effects of other opiods
Naloxone only partially reverses effects
Admin
Patch
Fentanyl
MOA
Powerful μ agonist
100x more potent than morphine
Administration
Sublingual tablets
Lozenges
Nasal spray
Patch
Indications
Moderate-severe pain
Severe acute somatic pain
Acute visceral pain
Pharmacokinetics
Hepatic metabolism
Renal excretion
Administrations
PO
IV
IM
SUblingual
Transdermal
Rectal
Adverse Effects
Respiratory suppression
Nausea and Vomiting
Constipation
Pruritus
Drowsiness
Hyperhidrosis
Hallucinations
Urinary retention
Opiod induced neurotoxicity
Withdrawal syndrome
Tolerance
Dependance and Addiction
over 3mnths ↑ risk of dependence
Falls
Coma
Death
Pharmacokinetics
Undergo Phase I and/or II
Opioid undergoing phase II metabolism have lower drug-drug interaction potential
Buprenophine metabolised by phase I and II
Interactions
Benzodiazepines / benz-like drugs
Addictive CNS depressant effects
↑ Risk of sedation, resp depression, coma, death
Cautions
Pt with hepatic / renal impairment
Elderly
Impaired resp function
Asthma
Hypoteniton
Urethral stenosis
Myasthenia gravis
Convulsive disorders
Chronic Non-Cancer Pain
Definition
Continuous or intermittent pain or discomfot persisting =>3 months for which painkillers have been taken and treatment sought recently and frequently
Associations
Depression
Sleep distubance
Fatigue
Reduced social integration
Reduced general functioning
Causes
Chronic Conditions
Nociceptive Pain
Osteoarthritis
Lower back pain
Neuropathic pain
eg. Post herpetic neuralgia
Both
No identifiable cause
Chronic pain after tissue damage or antecedent injury
Management
Relaxation therapy
Progressive muscle relaxation
Physiotherapy
Ocupation therapy
Nerve block therapy
Epidural pain relief therapies
Spinal cord stimulation
Pharmalogical Treatment
Antidepressants
Use
Neuropathic pain
Many non licensed for pain management
MOA
Independant of effect on depression
Lower dose
Drugs
Tricyclic
Notably used for neuropathic pain
Duloxetine
Licensed for diabetic peripheral neuropathy
Venlafaxine
Used unlicensed for neuropathic pain
Efficacy
50% experience relief
Discontinuation
Tapered off slowly to avoid CNS adverse effects
Antconvulsants
MOA
Ion channel interference
Reduced neuronal firing
Reduced pain sensation
Specific Anticonvulcansts
Carbamazepine
Indications
Trigeminal neuralgia
Peripheral neuropathy
Pharmacokinetics
Metabolised by CYP450 - interaction
Adverse Effects
Somnolence
Dizziness
Ataxia
Gabapentinoids
MOA
Bind α2-delta subunit of voltage gated Ca2+ channels
Decreases release of neurotransmitters: Glutamate, noradrenaline, substance P
Effects
Anticonvulsant
Analgesic
Anxiolytic
Gabapentin
Adverse effects
Resp depression
Dizziness
Somnolence
Headaches
GI
↑ Risk of suicidal behaviour and abuse
Neonatal withdrawal syndromes
Cautions
Misuse / abuse
Dependence
Renal impairment
Monitoring
Risk assesment
Monitoring of misuse
Monitor withrawal symptoms on discontinuation
Pregabalin
Adverse Effects
Severe respiratory depression
Cautions
Compromised respiratory function
Respiratory or neurological disease
Renal impairment
Concomitant use of CNS depressants
Older than 65 yrs
NICE chronic pain guidline
DO NOT initiate for pts 16 and over:
Antiepileptic drugs
Including gabapentinoids
Antipsychotics
Benxodiazepines
Corticosteroid trigger point injections
Ketamine
Local anaethetics
LA / Corticosteroid combo in tigger point injections
NSAIDs
Opioids
Paracetamol
Migraine
Definition
Primary headache disorder characterised by recurrent episodes of head pain with associated neurological, gastrointestinal and autonomic symptoms
Critera for Diagnosis
A. At least 5 attacks fulfilling criteria B-D
B. Headach attacks lasting 4-72 hrs
C. 2 of the 4 following
Unilateral pain
Pulsating quality
Moderate or severe intensity of pain
Aggravation by or causing avoidance of routine physical activity
D. One of the following
Nausea +/- vomiting
Photophobia and phonophobia
E. Not better accounted for by another diadgnosis
Epidemiology
Prevelance
More common in females
Lifetime prevelance of 43% among females age 15-49
30% exprience aura
Frequency
1-2 attacks per month
Pathophysiology
Neurology
Cortical
Subcortical
Brainstem neurons
Phases
Prodromalphase
Aura phase
Associated cortical spreading depression
Headache phase
Invloves activation of trigeminal sensory pathways
CGRP
Increased in pt
Believed to activate related pathways
Causes
Genetic and environmental factors
Triggers
Stress
Female hormonal changes
Change in lifestyle
Strong odours
Environment - bright light, weather
Caffeine
Excessive alcohol
Medication
OCP
Nasal decongestants
Management
Diet
Regular eating
Avoid known food triggers
Avoid processed food
Hydrate
Stress
Regular exercise
Maintain regular sleeping pattern
Modify work environment
Control triggers in times of hormonal changes
Acute Migraine Goals
Treat quickly
Achieve complete pain relief
Reduce incidence of adverse events
Acute medication should be used no more than 6-8 days per month
Avoid routine used of analgesics / opioids
Pharmacological Treatment
Prophylaxis
Anticonvulsants
Topiramte
Adverse Effects
Paraethesia
Cognitive dysfunction
Weight loss
Renal stones
Glaucoma
Teratogenic 🕷️
WOCBP need effective contraception
Antidepressants
Amitriptyline
Adverse Effects
Drowsiness
Antihypertensives
β Blockers
Propanolol
Metopropol
Ca2+ channel blockers
Flunarazine
ARBs
Candesartan
Anti-histamine
Pizotifen
MOA
Antihistamine
Serotoninergic antagonist properties
Adverse Effects
Wight gain
Sedation
Insufficient evidence for use
Acute
NSAIDs 🥇
1st line
Cautions
Uncontrolled hypertension
CVD
Risk of CVD
Efficacy improved with anti-emetics
Paracetamol
Indications
Mild-moderate attacks
Use
Combine with anti-emetics
Triptans 🥇
MOA
Highly selective 5-HT receptor agonist
1st line unless contraindicated
Contraindications
Hx of MI
CVD
Uncontrolled hypertension
MAOIs
Types
Sumatriptan
Zolmitriptan
Frovatriptan
Eletriptan
Almotriptan
Naratriptan
Administration
PO in mild N+V, start of headache
Rectal
Intranasal
Adverse effects
Flushing
Sensations of heaviness
Efficacy
Monotherapy effective in 30%
Consider dose increase, alternative triptan, combintations
Mentrual-Related Migraine
Long Acting Triptans
Naratriptan
Frovatriptan*
Unlicensed
Specialist Centres
Greater occipital nerve blocks for chronic migraine
Botulinum A
Monoclonal antibodies for CGRP
Fremanezumab
Erenumab
Galcanezumab
Eptinezumab
