PAIN Flashcards
(52 cards)
What is pain?
- an unpleasant sensory & emotional experience
- a/w actual/potential tissue damage
Classification of pain? (duration & pathophysiology)
Duration
- acute
- chronic
- breakthrough
Pathophysiology
- nociceptive (split into somatic & visceral)
- neuropathic
Diff between acute and chronic pain? (in terms of onset)
Acute: recent onset & probable limited duration
Chronic: last >3-6m or persists beyond duration of an acute disease, or after tissue healing is complete
Diff between acute and chronic pain? (in terms of type of pain)
Acute: nociceptive usually, but can be neuropathic
Chronic: nociceptive, neuropathic or both
Diff between acute and chronic pain? (in terms of sx)
Acute: sharp, dull, shock-like, tingling, shooting, radiating, fluctuating in intensity, varying in location (timely r/s with obvious noxious stimuli)
Chronic: same as acute but no timely r/s, pain stimulus may cause sx that completely change (e.g. sharp to dull)
Diff between acute and chronic pain? (in terms of signs)
Acute: can cause HTN, tachycardia, diaphoresis, mydriasis, pallor
Chronic: comorbid conditions often present, whatever listed in acute is seldom present
Diff between the cause of neuropathic and nociceptive pain?
Neuropathic: caused by lesion / disease of somatosensory nervous system
Nociceptive: arises from actual / threatened damage to non-neural tissue, due to activation of nociceptors in an individual with a normally functioning somatosensory nervous system
Features of neuropathic, somatic & visceral pain?
Where somatic & visceral pain arise from, characteristics of each pain
Neuropathic: burning, sharp stabbing pain, like electric shock (hyperalgesia or allodynia)
Somatic: arise from damage to body tissues, sharp / hot / stinging, localised
Visceral: arise from viscera mediated by stretch receptors (from internal organs), usually accompanied by N/V
What is hyperalgesia and allodynia?
Hyperalgesia: exaggerated painful responses to normally noxious stimuli
Allodynia: painful responses to normally non-noxious stimuli
What is SOCRATES used for and what does it stand for?
Used for pain hx taking
Site
Onset
Characteristics
Radiation
Associated sx
Time course
Exacerbating / relieving factors
Severity
What are the pain scores used to assess pain?
- numeric rating scale
- verbal descriptor scale
- faces pain scale
What is the pain ladder from WHO?
- non-opioid +- adjunvant
- opioid for mild-moderate pain +- non-opioid +- adjuvant
- opioid for moderate-severe pain +- non-opioid +- adjuvant
What are non-opioids?
Paracetamol, NSAIDs
What are weak and strong opioids?
Weak: tramadol, codeine etc
Strong: morphine, fentanyl etc
When is paracetamol absolutely CI and cautioned in?
CI: Liver failure
Caution: hepatic insufficiency, chronic alcohol abuse or dependence
When is NSAIDs CI?
- GI ulcer/bleed
- asthma
- pregnancy 3rd trimester
- kidney problem
- CVD (uncontrolled HTN, HF, IHD)
- allergy
- liver problem
- bleeding disorder / meds
What are the greatest risk a/w COX-1 and COX-2 inhibition activity?
COX-1: upper GI bleed/perforation
COX-2: CVD
Do NSAIDs help with non-specific low back pain?
No
Is celecoxib or etoricoxib more COX-2 selective?
Etoricoxib
Selectivity from COX-1 to COX-2? (12 drugs)
Ketoprofen, piroxicam, indometacin, aspirin, naproxen, ibuprofen, diclofenac, mefenamic acid, meloxicam, celecoxib, parecoxib, etoricoxib
NSAIDs MOA?
Block COX (which breaks down AA to prostaglandins TXA2, PGE2, PGI2)
Function of PGI2, PGE2 and TXA2?
PGI2: vasodilation, inhibit platelet aggregation
PGE2: vasodilation, vasoconstriction, vascular permeability (swelling), pain
TXA2: vasoconstriction, platelet aggregation
MOA of codeine?
weak mu & delta opioid agonist -> metabolised to morphine by CYP2D6
MOA of tramadol?
weak mu opioid agonist & inhibit reuptake of NA & serotonin
