1: Pain Management Flashcards
define pain and distinguish between acute and chronic pain
pain is an unpleasant sensory and emotional experience associated with actual or potential tissue damage
- acute: painful with rapid onset/short course
- chronic: painful persisting beyond the normal time of healing
how is pain transmitted
nociceptors
what are nociceptors
free nerve endings of afferent neurones that transmit pain perception via spinothalamic tract
what do nociceptors respond to
- mechanical deformation (e.g. severe pressure)
- excessive heat
- certain chemicals
- neuropeptide transmitters e.g. bradykinin, histamine, cytokines, prostaglandins)
all sensory information transmitted to the CNS can be modulated - how can afferent neurone transmission be inhibited
- collateral branches of other ascending neurones
- cerebral cortices via descending neurones
- specific synapses (indirect inhibition)
how is pain modulated (3)
- afferent input from nociceptors is continually inhibited
- allows ‘disinhibition’ during severe tissue damage which increases pain signal
- allows complete inhibition to completely block pain signal
how can pain be augmented
- emotion e.g. anxiety
- suggestion
- activation of other sensory modalities
what are risk factors for developing chronic pain
patient factors
- pyschological
- female
- younger age
- genetics
- depression
medical factors
- repeat surgery
- nerve damage
- RT to area
- duration of postop pain treatment
what is hyperalgesia
increased pain sensation to the same stimulus (pain perception disproportionate to the stimulus)
what is allodynia
sensation of pain in absence of painful stimulus
what are the benenfits of post-op analgesia
- ↓ sympathetic effects of pain
- earlier mobilisation
- ↓ risk of post op resp complications
- ↓ chronic pain syndromes
what key aspects of assessment of pain
-
history
- SQITARS
- effects on function
- response to treatment
- medical/surgical hx -
examination
- obs e.g. HR, BP, RR
- spO2 - pain may lead to desaturation in adults
- exam of painful site
- mobilising without pain?
- deep breathing
- able to eat/drink where appropriate -
qualitative
- pt describes pain
- appearance e.g. sweating, distress -
pain measurement tools
- categorical scales
- VAS
- NRS
- paediatric faces
WHO pain ladder
minimal side effects but most analgesic benefit
what is the MOA of paracetamol
? inhibits PG synthesis in CNS
? modulates endogenous cannabinoid system
what are the side effects of paracetamol
- CVS: hypotension and bradycardia if given rapid IV
- CNS: analgesia and antipyretic
- rare: rash, idiopathic thrombocytopenia
what is the absorption/distribution of paracetamol
- absorbed in small bowel
- 80% oral bioavailability
- 10% protein bound
what is the dosing of paracetamol
- adults >50kg: 1g, 6 hourly
- children & adults <50kg: 15mg/kg 6 hourly
what is the metabolism/excretion of paracetamol
- hepatic metabolism to glucoronide, excreted in urine
- 10% metabolised by P450 system to toxic NAPQI (genetic enzyme polymorphism determines amount of NAPQI produced)
- normal dose: NAPQI conjugated by glutathione and harmless product excreted in urine
- overdose: glutathione exhausted and NAPQI accumulation –> liver failure
what is the MOA of NSAIDs
inhibits cyclo-oxygenase which reduces the production of inflammatory prostanoids e.g. PG, thromboxane, prostacyclin
what is the function of prostacyclin
- vasodilator
- prevents platelet plug formation
what is the function of thromboxane
- vasoconstrictor
- potent platelet aggregator
what are the functions of various PGs
- PGE2: ↓ gastric acid secretion, ↑ gastric mucous secretions
- PGI2: vasodilation, platelet aggregation
- PGF2: uterine contraction, bronchoconstriction
what is the mechanism of NSAID-induced asthma
leukotriene production ↑ due to COX inhibition
give examples of non-selective COX inhibitors
aspirin
ibuprofen
diclofenac
give an example of a selective COX-2 inhibitor
parecoxib
how are NSAIDs absorbed/distributed
- significant first pass metabolism, well absorbed by all routes
- highly protein bound
how are NSAIDs metabolised/excretion
hepatic metabolsim, excreted in bile
what are the side effets of NSAIDs
- bronchospasm sensitivity in 20% asthmatics
- ↓ PG required to maintain gastric mucosal intregity
- PG & prostacyclin inhibition –> local hypoxia and ↓ renal perfusion for potential for AKI
- reversible inhibition of platelet function
what are opioids
synthetic substances that stimulate opioids receptors e.g. fentayl, alfentanil
give 4 types of opioid receptors
- MOP µ
- KOP k
- DOP δ
- NOP (nociceptin)
what is tolerance
decreasing response to repeated dosing of drug - over time a larger dose is required to produce the same effect
what is dependence
requirement for repeated administration of a drug to avoid withdrawal symptoms
what is addiction
patient’s behaviour as a result of their drug dependence e.g. lack of control, cravings, drug-seeking, compulsiveness
state some opioid withdrawal symptoms
- anxiety and fear
- adrenergic hyperactivity
- malaise
- abdo cramps
- sweating
- yawning
what is the MOA of morphine
MOP & KOP agonist - stimulates pre-synaptic GPCRµ
- closure of VGCC
- ↓cAMP production
- K+ efflux
- hyperpolarisation of cell membrane
- ↓ excitability of the cell - ↓NT release - reduced pain transmission
what is the absorption/distribution of morphine
- good oral absorption from SB - extensive first pass metabolism
- 15-20% oral F, 20-40% protein bound
- peak effect 10-30 mins, duration 3-4 hours
what is the metabolism/excretion of morphine
- hepatic metabolism to morphine-3-glucuronide (inactive) and morphine-6-glucoronide (x13 potency)
- ‼️ liver impairment
- excreted in urine - active metabolites accumulates in renal failure
what are CVS side effects of morphine
- no direct effects
- hypotension if histamine release occurs
- mild bradycardia due to ↓ sympathetic tone
what are respiratory side effects of morphine
- dose dependent resp depression
- ↓sensitivity to rising pCO2
- antitussive
- bronchospasm if histamine release
what are CNS side effects of morphine
- analgesia
- sedation
- euphoria
- hallucinations
- meiosis via EDW nucleus
- seizures/muscle rigidity at high doses
what are GI side effects of morphine
- ↓ motility
- ↓ gastric acid, pancreatic, bile secretions
- N&V - CTZ stimulation via 5HT3 & dopamine receptors
GO
what are GU side effects of morphine
↑ tone in bladder detrusor and sphincter muscles - urinary retention
what are skin side effects of morphine
rash
pruritus
what are endocrine side effects of morphine
- ↓ACTH
- ↓ gonadotrophic hormones
- ↑ ADH causing hypernatremia & water retention
what is regional analgesia
targeted analgesia depending on specific surgery e.g. complexity, site, etc
- optimises peri-op analgesia to enhance recovery & reduce requirement for systemic meds esp opiates
give 3 subtypes of regional analgesia
- neuraxial blocks e.g. spinal (intrathecal morphine single shot), epidural (thoracic/lumbar)
- truncal regional nerve blocks e.g. TAP, rectus sheath block +/- continuous infusion via nerve catheter, ilioinguinal
- peripheral nerve blocks e.g. fem/pop, brachial plexus
