Flashcards in Pain Deck (33):
Types of pain:
Stimulation of peripheral noiceptors
Limb fractures, sprains, burns
Types of pain:
Neuronal damage by inflamation
Post-herpetic neuralgia, cancer pain, diabetic neuralgia
Types pf pain:
Physical pain from emotional factors
Tension headache, back pain, stomach pain
Types of pain:
Pain from removed limb
Why do we have pain?
Pain signals to brain that body has encountered a damaging stimulus
What two diseases improperly perceive pain?
Familial dysautonomia (disorder of ans)
Congenital insensitivity to pain and anhidrosis (mutation in ntrk1r for ngf)
How are pain pathways activated, ie. what threshold and firing rate?
High and fast
Types of nociceptors
Gpcr, ligand gated, heat/acid sensing trp, heat sensitive k+ channels
A delta fibres
Conveys 10% of pain
90% of pain
Reticular formation of brain
General onset of pain
Origin of descending analgesic pathways
Spinothalamic tract, sends efferents to map pain
Relays between ascending and descending pathways
Lesion does not increase pain threshold or reduce analgesia
Under what may pain be supressed?
Stress induced analgesia in mice is partially blocked by naloxone mu opiod antagonist
Brain areas involved in descending pain pathways
Rostral ventral medulla
Contain lots of opiod receptors
Role of descending pathways in pain
Descend to spinal cord and inhibit release of substance p
How do opiods work?
Inhibit gaba inhib interneurones on descending pathway, therefore increase descending excitation into spinal cord to suppress pain.
Enkephalins, dynorphin, endorphin
Anandamide and 2-aracidonyl glycerol
Stress induced analgesia partially blocked by rimonabant
Asprin, ibuprofen, naproxen, indomethacin
Role of nsaids
Decrease inflammation, decrease sensitiation, decrease fever (antipyretic)
Analgesic effects of paracetamol and nsaids
Decrease synthesis of proinflammatory prostaglandins and pro-nociceptive compounds from arachidonic acid via inhibition of cox-1 and cox-2 enzymes
Mechanism of action of nsaids
Tissue injury, membrane breaks down to release arachidonic acid
Which with the use of cox1 and cox2 makes prostaglandins
Prostaglandins are isomerised in specific tissues (platelet aggression, sensitisatio of noiciceptors)
Role of cox1
Products protect the stomach from acid enviornment
Blocked by asprin, non selective nsaids
Role of cox2 and inhibitors
Products recruit inflamation, wbcs, sensitise oain, stimulate fever
Blocked by asprin, nonselc nsaids, cox inhibs
Cox2 selective inhibitors discuss.
Increase formation of thromboxane
Decrease formation of protective prostacyclin
Increase cardio risks
Not an nsaid
Does not decrease inflamation but is an analgesic
Interacts with cox enzymes at different sites to nsaids?
Or interacts with endocannabinoid system?
Why dont you take paracetamol with alcohol?
Both metabolised by liver enzyme cytochrome p450
By products are free radicals, these require endogenous antioxidants (glutathione) in liver
But these are saturated
What is referred pain?
Tissue damage in viscera feels like its coming from bodys surface
Mechanism of refered pain
Neurones from viscera and skin synapse on the same dorsal horn neurone
Brain cannot distinguish location of pain
What is sensitisation?
Damaged tissue releases inflam mediators that decrease activation threshold of nociceptors
Activation threshold of noicipetors is lowered
Pain extends beyond area of tissue damage
Protective mechanism but may be bad long term as receptor population in dorsal horn changes