Analgesics Flashcards
What 3 reasons can be pain be useful for?
Warning individual there is a problem
Assisting clinician in localising pain
May help with diagnosis
What is a common and distressing symptom of many illnesses and diseases?
Pain
What uses a receptor to detect it and also needs pathways to the brain to inform the patient that there is a stimulus causing it?
Pain
What are nociceptors?
Receptors that detect pain
What are receptors that detect pain called?
Nociceptors
Do nociceptors have high or low thresholds?
Why?
High - so only detect stimulus that is potentially tissue damaging
What 3 types of damage do nociceptors detect?
Mechanical
Thermal
Chemical
What are the 3 sensory afferents?
AO Fibres
C Fibres
AB Fibres
What type of damage do AO Fibres detect?
Mechanical, thermal and chemical
What type of damage do C fibres detect?
Mechanical, thermal and chemical
Which fibres detect pressure, touch and position?
AB fibres
Which fibre detects sharp, well-localised pain?
AO fibres
Which fibre detects dull pain?
C fibres
What happens to AO and C fibre pathways when the AB pathway is stimulated?
It can marginally interfere with the others - modulating pain
What is the gate control theory of pain?
Rubbing an area - this stimulates the AB pathway and modulates pain caused by the other two pathways
What is the thickest/biggest and fastest sensory afferent pathway?
Which is the slowest and smallest?
AB is fastest (touch) Then AO (sharp localised pain) Then C (dull pain)
Which sensory afferent pathways are myelinated?
AO and AB
How does the pain/touch stimulus reach the sensory cortex?
It goes to the dorsal horn, spinothalamic tract, ventral posterior lateral nucleus (thalamus) then the sensory cortex
Horn-Tract-Thalamus-Sensory Cortex
What are the main 4 things that activate action potentials and cause inflammation, as a response to pain?
B5PH
Bradykinin
5-HT
Prostaglandins
Histamine
What do nociceptors release to cause inflammation, that act on the mast cells to produces histamine and blood vessels to produce oedema?
CGRP
Substance P
What would reducing the production of Bradykinin, 5-HT, Prostaglandins and Histamine do?
Prevent/reduce inflammation
What is the main part of the inflammatory ‘soup’ that we need to inhibit in order to stop the action of other mediators?
Prostaglandins
What sensitises afferent C fibres to bradykinin?
Prostaglandins
What drugs inhibit prostaglandin production?
NSAIDs
Non-Steroidal Anti-Inflammatory Drugs
What do NSAIDs need to inhibit in order to inhibit the production of prostaglandins?
COX 1 and COX 2 - as they are needed to produce them
Which COX enzyme is responsible for pain and inflammation?
COX2
What are the 4 pharmacological reactions of NSAIDs?
Antipyretic
Analgesic
Anti-inflammatory
Musculoskeletal Pain
What drugs can be used as antipyretic, analgesics, anti-inflammatory and to combat musculoskeletal pain?
NSAIDs
What does antipyretic mean?
To reduce body temperature during fever
What is the name for when a drug reduces body temperature during fever?
Antipyretic
When we say a drug provides the relief of pain associated with the increased production of PGs (such as arthritic, muscular, dental pain etc) what do we say it is?
An analgesic
What are arthritic, muscular, dental pain, post-partum and bone cancer pain examples of?
What treats it?
Pain produced by increased prostaglandins.
NSAIDs can act as an analgesic for this
When a drug reduces oedema and the sensitisation of nociceptors, what do we call this and what drug can do this?
Anti-inflammatory
NSAIDs
What is chronic treatment?
An increased dosage of drug or prolonged treatment
What are the side effects of NSAIDs if they are used as a chronic treatment?
(e.g. for chronic arthritis)
DINVUG
Indigestion, diarrhoea, nausea, vomiting, gastric bleeding and ulceration
What area do the negative side effects of NSAIDs tend to affect?
The GI Tract
Explain how long-term NSAID use can cause GI tract side effects:
NSAIDs inhibit COX 1, which synthesises certain prostaglandins (PGI2 and PGE2) that are important for mucus and HCO3/bicarbonate secretion - these help decrease acid secretion and increase blood flow to the stomach to protect it.
Inhibiting COX1 stops this protection = ulcers etc
NSAIDs bind to COX 1 and COX 2 - what are the results of this?
COX 2 = reduces pain and inflammation - good
COX1 = reduces mucus and bicarbonate secretion = more acid and less blood flow in stomach - bad? GI side effects
What are celecoxib and etoricoxib?
Pay attention to COX in name.
What is good about them?
They are NSAIDs that only inhibit the COX2 enzyme - reducing side effects.
Can cause MI however.
Most NSAIDs inhibit both the COX 1 and 2 Enzyme.
What 3 ways can reduce the negative side effects of this?
E P P
Enteric Coating of Tablets (protects stomach lining from effects)
Protective Agent - give with another drug: Misoprostol (prostaglandin analogue) or Omeprazole (Proton Pump Inhibitor)
Pro-Drugs - must be metabolised before it works
e.g. sulindac, nabumetone, fenbufen