wk 2- analegesic, anesthetic, sedatives Flashcards
types of pain/ classification of pain
- acute- less than 30 days, pathology clear, treatment typically analegics
can be
nocieptive
inflammatory
neuropathic - chronic- constant 3months or longer in the past 6 months, pathology unclear
can be
central pain
non neuropathic
neuropathic
psychogenic
treatment of nociceptive pain vs neuropathic
nociceptive- sharp, dull, aching pain that can radiate
-NSAIDS and OPIODS
neuopathic- tingly, burning, shooting pain
-Resistant to NSAIDs
-TCAs, anticonvulsants, sodium channel blockers
impacts of pain
- inability to work
- quality of life
- loss of worth and self esteem
- sleep disturbance
- mood, depression, suicidal
- health status reduced
- unable to exercise
- fatigued
types of analgesics podoatrist can prescribe
- non opioid analgesics
- aspirin
-paracetamol - opoiod
- codeine
-oxycodone (surgeon) - NSAIDS
-celecoxib
-diclofenac
-ibuprofen
-indometacin
-meloxicam
-naproxen
-sulindac
-ketorlac (surgeon)
acute pain - treatment options and how to treat different severities of pain
- NSAIDS with or without paracetamol
- opioids
mild- non opioid (paracetamol, NSAIDS, aspirin) with or without adjuvant
mod- weak opioid added like codeine
severe- strong opioid instead of weak like oxycodine
paracetamol indications, contrindications, overdose levels
analgesic, anti pyretic, mild anti inflammatory
indications- mild to mod pain in isolation or combined
contraindicated in-
infants less than 1 month
hepatic/renal impairment
allergy
3x500mg every 4-6 hours max
which is max 4g daily- build up of toxic metabolites
NSAIDs MOA, indications, contraindications
Analgesic, anti inflammatory and antipyretic
MOA- inhibit COX enzyme, reduce prostaglandins
indicated in- pain with inflammation, arthritis/MSK conditions
contraindication in-
peptic ulcers/GI bleeding
asthma
renal/hepatic impairment
hypertension/fluid retention
chronic congestive heart failure
large amount of drugs
alcohol, anticoagulants, antacids, antihypertensives, diuretics, lithium, MTX, NSAIDS, sulfonylureas, cyclosporin
infection/inflammatory response
triple whammy (ACE, NSAID, DUIETRIC)
COX 1 ENZYME
stomach lining
cox 2 enzyme
inflammatory process and platelet aggregation
NSAIDs can be
cox2 selective or non selective (1/2)
what do cox2 selective NSAIDS do
also are anti inflammatory/fever and pain relivers but cause fewer stomach and intestinal problems (bleeding, ulcers, sodium retention, renal function) by not inhibiting cox1 responsible for lining the stomach
example of cox2 selecetive NSAIDS (coxib)
- ibuprofen
- diclofenac- topical
- naproxen
- mefenamic
adverse effects of NSAIDS
GI bleeding
renal and hepatic disturbances
CVD risk
asthma worsened
rash- topical
triple whammy
ACE
DIURETIC
NSAID
renal failure
what NSAIDS are first choice for inflammatory joint disease and why
ibuprofen, fenbrufen, naproxen less side effects
a drug that combines paracetamol/ibuprofen
maxigesic
opioids MOA, indications, contraindications
moa- mimick natural ligands for opioid receptors in brain and spinal cord, Mu receptor mostly for analgesia (endorphin, enkephalin)
indications- mod-severe pain
contraindicated in- addiction/dependence
adverse effects of opioids
with long term use:
tolerance
dependence/addiciton
opioid induced hyperalgesia
endocrine disorders
constipation
nauesea
pruritius (itching)
what are adjuvant analgesics?
antidepressants and anticonvulsants
most effective in nociplastic nerve pain (neuropathic pain)/ sleep depletion due to pain
adverse effects of antidepressents
sedation, dry mouth, blurred vision, constipation, weight gain, arrhythmias, orthostatic hypotension
adverse effects of anticonvulsants (antiepiletic drugs)
drowsiness
nausea
falls/blurry vision
weight gain
cognitive dysfunction
suicidal
convulsions
local anaesthesia MOA
reversible loss of sensation in an area of the body
block sodium ion channels so that sodium cannot flow into neurons inhibiting the transmission of APs along individual neurons
what nerves are more susceptible to LA
small fibres and myelinated neurons
differences between esters and amides LA
esters
short-long duration
metabolised rapidly by enzyme in blood/skin
possiblity of allergic reaction
photo/temperature labile
slower onset
pka- weak base
amides
longer duration
metabolised slower by liver
mod-fast onset
pka- closer to neutral
amide more preferred because of its rapid onset and stable compound, less likely to cause reaction
order nerves are blocked by LA
smaller myelinated fibres blocked first because more sensitive
autonomic (B)
sensory (A)
motor fibres (C)
components of LA molecule and what they do
aromatic ring- confers lipid solubility
intermediate linkage- dictates mode of metabolism (ester/amide)
terminal amine- charged or uncharged for water solubility
what are LAs pH and why is it important
weak bases, they exist in both ionised and unionised forms but only the unionised form can reach its site of action then it needs to become ionised to bind to sodium ion channels
amide LA
bupivacaine
lidocaine
ropivicaine
etidocaine
ester LA
cocaine
chloroprocaine
tetracaine
procaine
important clinical properties of LA
onset
potency
duration of action
potency means
concentration of rug required to produce effect
onset means
length of time it takes for medicine to work
complications of LA
-broken needles
-wrong solution
-injection into blood vessel
-infection
-neuralgic pain
-nerve palsy
allergies to LA
allergy to LA is rare
allergies are usually related to
psychogenic
presevatives / latex
cardiovascular response to adrenaline
allergies are more common in
esters
sedatives/hypnotics podiatrist can prescribe
diazepam
lorazepam
benzos (sedatives/hypnotics) MOA
increase effectiveness of endogenous inhibitory neurotransmitter GABA
