Here are some elements of this response:

Damaged sensory hairs (stereocilia) of the hair cells; damaged hair cells degenerate and die. In humans and other mammals, dead hair-cells are never replaced; the resulting hearing loss is permanent. Inflammation of the exposed areas. This inflammation causes poor blood flow in the exposed blood vessels (vascular stasis), and poor oxygen supply for the liquid inside the cochlea (endolymphatic hypoxia) Those noxious conditions worsen the damaged hair cell degeneration. Synaptic damages, by excitotoxicity. Noise overstimulation causes an excessive release of glutamate, causing the postsynaptic bouton to swell and burst. However the neuron connection can be repaired, and the hearing loss only caused by the "wiring" (i.e. excitotoxicity) can thus be recovered within 2–3 days. Hair cell damage or death
When the ear is exposed to excessive sound levels or loud sounds over time, the overstimulation of the hair cells leads to heavy production of reactive oxygen species, leading to oxidative cell death. In animal experiments, antioxidant vitamins have been found to reduce hearing loss even when administered the day after noise exposure. They were not able to fully prevent it. Antioxidants however do not seem to be effective in protecting the human ear. Damage ranges from exhaustion of the hair (hearing) cells in the ear to loss of those cells. NIHL is, therefore, the consequence of overstimulation of the hair cells and supporting structures.
An acoustic signal from a sound source, such as a radio, enters into the external auditory canal (ear canal), and is funneled through to the tympanic membrane (eardrum), causing it to vibrate. The vibration of the tympanic membrane drives the middle ear ossicles, the malleus, incus, and stapes to vibrate in sync with the eardrum. The middle ear ossicles transfer mechanical energy to the cochlea by way of the stapes footplate hammering against the oval window of the cochlea, effectively amplifying the sound signal. This hammering causes the fluid within the cochlea (perilymph and endolymph) to be displaced. Displacement of the fluid causes movement of the hair cells (sensory cells in the cochlea) and an electrochemical signal to be sent from the auditory nerve (CN VIII) to the central auditory system within the brain. This is where sound is perceived. Different groups of hair cells are responsive to different frequencies. Hair cells at or near the base of the cochlea are most sensitive to higher frequency sounds while those at the apex are most sensitive to lower frequency sounds. There are two known biological mechanisms of NIHL from excessive sound intensity: damage to the structures called stereocilia that sit atop hair cells and respond to sound, and damage to the synapses that the auditory nerve makes with hair cells, also termed "hidden hearing loss". Physiological response
The symptoms mentioned above are the external signs of the physiological response to cochlear overstimulation.