1 - Introduction To Oral Physiology
1 - Introduction To Oral Physiology
1 - Introduction To Oral Physiology
Tahani Abualteen
/72
Aspirin blocks the chemical receptors that are involved in pain sensation by blocking the pathway that leads to the formation of the previous products (especially prostaglandins) Aspirin inhibits an enzyme called cyclo-oxygenase which is important in the process of formation of pain stimulants (e.g. Prostaglandins), and when this happens; pain is lost Aspirin is not used that much because its an anticoagulant (prevents blood coagulation) Safer drugs to use include non-steroidal anti-inflammatory drugs (e.g. Ibuprofen)
Nociceptors: o Touch & temperature receptors are well defined o Nociceptor is a term used to describe a nerve ending that responds to stimuli that actually or potentially produce tissue damage o Pain receptors (nociceptors) respond to painful stimuli o Nociceptors may respond to very gross mechanical stimuli If the mechanical stimulus is very intense and able to produce tissue damage, then nociceptors may respond to it although touch receptors are the one responsible for mechanical stimuli o Other stimuli may result in painful sensation when level of stimulus is increased For example if hand is put in a warm water, then thermal receptors will tell the brain that this water is warm If the stimulus is more intense (the water isn't just warm, it is boiling) then when hand is put, thermal receptors will respond and also nociceptors since some tissue damage was produced o A single noxious heat stimulus is sensed as painful o Repetitive stimulation of temperature receptors with less powerful stimuli may inhibit the passage of pain
/74
For example: suppose you are walking in your home, when suddenly your foot hits something like a table or a chair and it's too painful, what you will actually feel are two types of pain The first (initial) pain is felt due to A fibers because they are the faster ones producing stinging pain (sharp of high intensity) Then the second pain is felt due to C fibers because they are the slower ones producing agonizing intolerable diffuse pain C fibers are Unmyelinated and thus pain impulses travel through them very slowly A fibers: o o o o o o Myelinated (2.5 m) Conducting at 12-30 m/s High threshold to be stimulated, the stimulus has to be very intense and higher than the threshold Transmit information from nociceptors or mechanoreceptors Activated by intense mechanical stimulation Involved with 1st pain Sharp localized sensation from obvious mechanical damage and lasts for less than one second
Pain neuron: o Neuron Cell body and dendritic processes Axon o Neurons conducting pain travel along three levels Primary Secondary Tertiary Cell bodies in - Posterior root ganglia of spinal cord OR - Ganglia of cranial nerves Ganglia = aggregation of cell bodies in the PNS In the cranial area; all primary neurons conduct pain from pain receptor nerve endings to the Spinal Nucleus of Trigeminal nerve irrespective of the cranial nerve of origin From Spinal Nucleus of Trigeminal nerve to thalamus From Thalamus to cerebral cortex
o Primary neuron
o Secondary neuron o Tertiary neuron Factors affecting pain threshold: o Factors lowering threshold so that small stimulus is needed to produce pain sensation Psychological factors Fear & worry Excitement & relaxation Soothing (relaxing) music
o Factors elevating threshold so that intense stimulus is needed to produce pain sensation
Nerve Physiology: Nerve cell axon is the area where pain impulses are conducted and travel Intracellular Fluid (inside the axon) Extracellular Fluid (outside the axon)
/76
Depolarisation: o Action Potential and Depolarisation: Rapid fall in membrane potential from 70 to +20 - 30 mV Nerve impulse (action potential) propagates along the axon and when it reaches the resting segment of the axon it creates an electrical stimulus which increases the permeability of the diffusion barrier to Na and K ions by opening voltage gated ion channels Na+ ions move into cell while K+ ions move out along concentration gradient (without energy) Intracellular charge is now positive relative to extracellular This segment of the axon has undergone depolarisation and is in a state of action potential As depolarisation progresses along the axon, the action potential is propagated and the nerve stimulus continues down the length of the axon Repolarisation: o The axon returns to its original state with initial concentrations of Na and K ions restored and the interior once again negative relative to the exterior o This is achieved by the Na and K channels o The axon is ready to undergo depolarisation again to propagate a nerve impulse o Active process that takes up energy
Mechanism of action of local anaesthesia: o Blocking of the Na ion pumps in the cell membrane wall o This results in an inability for Na ions influx when the action potential arrives at a given segment of the nerve o No effect on resting potential
/77