Pain Management Flashcards
What are the three types of pain?
Nociceptive pain
- Associated with the detection of potentially tissue-damaging noxius stimuli and is protective
Inflammatory pain
- Associated with tissue damage and the infiltration of immune cells and can promote repair by causing pain hypersensitivity until healing occurs
Pathological
- A disease state caused by damage to the nervous system (neuropathic) or by its abnormal function (dysfunctional)
What is Allodynia?
Pain from something that isn’t normally painful
What are the three most common painkillers?
Paracetamol, NSAIDs and opioids
What is the difference between A fibres and C fibres?
(Pain nerve fibres)
A fibres
- Myelinated, fast, send impulses directly to the hypothalamus
- Carry a sharp acute easily localised pain
- Not from deep visceral organ
- Also responsible for lighter touch sensation
C fibres
- Unmyelinated, slower
- Carry a throbbing, aching, or chronic pain
- Can be from deep visceral changes
- Sense stimuli which then create an electrical signal which is then conducted into CNS
What do different nerve fibres respond to?
Merkels disk –> Fine touch or pressure
Free nerve ending –> Pain, heat/ burning or cold
Meissner’s corpuscle –> Light touch or pressure
Pacinian corpuscle –> Sustained pressure
Refini’s ending –> Pressure or distortion
What is inflammation?
A non-specific response of the body to injury with a role in initiating/ coordinating tissue repair
It is usually self-limiting (acute) but can sometimes be self sustaining (chronic) which can lead to ongoing damage
When does acute inflammation occur?
In a result of an injury or infection
Chemical messages by cytokines, are sent out which encourage WBC (neutraphils) to come to site to deal with problem and cause inflammation. Attracted by inflammatory chemicals (cytokines). Digest pathogenic cells and molecules.
Increased pressure in vessels force exudate from capillaries via larger endothelial clefts/ gaps (odema).
Increased blood flow, redness and heat.
Hyperaemia due to dilation of increased blood flow in capillaries - erythema, pyrexia
What are prostaglandins?
Umbrella term for COX enzymes and prostanoids
Lipid autocoids derived from Arachidonic acid.
Phospholipids from cell membranes are released into the tissue. Arachidonic acid (FA) from phospholipids starts being metabolised and changed by enzymes COX-1 and COX-2 (enzymes that change lipids) result changing lipids and producing lipid hormones called prostanoids.
They then sensitize nerve endings to pain and produce other mediators (chemical messengers) e.g. Bradykinin and 5-hydroxytryptamine. The production is sped up by COX enzymes
Depending on what lipids are present in cell membrane at the time, inflammatory or anti-inflammatory prostaglandins can be produced.
Lipid-based hormones
What is COX-1?
A physiologic (permanent) enzyme that is constantly responding to Arachidonic acid.
Expressed in stomach and other cells
Protects gastric mucosa
Involved in tissue homeostasis
Involved in prostaglandin production
What is COX-2?
An inducible (upregulated when required) enzyme that responds to Arachidonic acid when necessary.
Causes inflammation, pain, and fever.
Involved in prostaglandin production
How is inflammatory pain reduced?
Inhibit/ inactivate both COX enzymes (inhibit arachidonic acid production)
Reduce prostaglandin production
Reduce sensitivity of peripheral nerves to pain mediators
Inflammatory cytokines need to subdued, and interleukin 1 and TNFa.
How do NSAIDs drugs work?
Inhibit Cox-1 and/or Cox-2 enzymes
Actions include:
Anti-inflammatory
Analgelsic - pain relief
Antipyretic - lowers the temperature
Can cause peptic ulcers
What NSAIDs have the strongest side effects?
Aspirin, Ketoprofen
- Highly COX-1 selective (highest GI tract side effects)
Ibuprofen, Naproxen, Diclofenac
- Slightly COX-1 selective
Etodolac, Meloxicam
- Slightly COX-2 selective
Celecoxib
- Highly COX-2 selective (lowest GI tract side effects)
What can interact with NSAIDs?
Anticoagulants
ACE inhibitors
Diuretics
What are the risk factors for NSAID damage
- Advanced age
- HIstory of GI events
- Major organ impairment
- Use of high dose or multiple NSAIDs
Risk
Ketoprofen –> Indomethacin –> Naproxen –> Diclofencac –> Ibuprofen
