L14: Pain Flashcards
What are the 3 types of pain?
acute, chronic and intermittent
What is the disorder associated with loss of pain sensation?
CIPA
What causes CIPA?
mutation in gene for a nerve growth factor so sensory nerves don’t develop properly
What are the 3 classes of nociceptor? What are they activated by?
- thermal: activated by v high or low temps
- mechanical: activated by intense pressure
- polymodal: activated by high intensity mechanical, thermal, or chemical stimuli
What are C fibres and what signal travels along them?
unmyelinated axons - signal ongoing slow dull pain (polymodal receptors)
What are A∂ fibres and what signal travels along them?
thinly myelinated axons - signal acute onset (thermo & mechanoreceptors)
What type of receptors are usually featured on nociceptors? What stimuli are they sensitive to?
TRP (Transient Receptor Potential) channels - sensitive to lots of different stimuli
Describe the ascending somatosensory pathways for pain
dorsal root → synapse on dorsal horn of spinal cord projection neurons → cross midline → ascend to thalamus (via spinothalamic tract) → thalamic neurons project to somatosensory cortex and other nuclei involved in pain response ⇒ allows us to locate pain
What is hyperalgesia? What causes it?
- enhanced pain
- usually due to previous injury
- often due to inflammation and release of chemicals from damage site
What is allodynia?
- Pain in response to innocuous sensory stimuli
What is substance P? What does it do?
- local transmitter
- activates mast cells to release histamines → inflammation
How can hypergesia result in chronic pain?
strength of synapses in CNS changes→ sensitisation of networks in nervous system and brain → chronic pain [very complex]
Describe the gate control model, with examples
Pain signalling can be “gated” by stimulation of non-pain sensory fibres from same area which activates inhibitory interneurons in dorsal horn, reducing output of projection neurons = less excitable, less APs
- e.g. rubbing site of injury
- e.g. TENS (provides different signal from area → decreases pain system)
Are opioid receptors generally excitatory or inhibitory?
Inhibitory -> activation can lead to analgesic effects
How do NSAIDs work?
inhibit cyclooxyrgenase enzymes to reduce prostaglandin synthesis, have pain suppression effects both at site of injury and in sensory neurons in dorsal root ganglion (DRG) and CNS