Although occasionally preceded by and/or associated with vesicle formation, it is always associated with a juxta-epithelial inflammatory reaction followed by a fibroelastic change of the lamina propria with epithelial atrophy leading to stiffness of the oral mucosa, progressive decrement in mouth opening and inability to eatPer Chandramani More and Naman Rao (2019) (Clinical definition)-
A debilitating, progressive, irreversible collagen metabolic disorder induced by chronic chewing of areca nut and its commercial preparations; affecting the oral mucosa and occasionally the pharynx and esophagus; leading to mucosal stiffness and functional morbidity; and has a potential risk of malignant transformation. Epidemiology
The incidence of the disease is higher in people from certain parts of the world including South and South East Asian, South Africa and the Middle Eastern countries. Symptoms
In the initial phase of the disease, the mucosa feels leathery with palpable fibrotic bands. In the advanced stage the oral mucosa loses its resiliency and becomes blanched and stiff. The disease is believed to begin in the posterior part of the oral cavity and gradually spread outward. Other features of the disease include: 

Xerostomia
Recurrent ulceration
Pain in the ear or deafness
Nasal intonation of voice
Restriction of the movement of the soft palate
A budlike shrunken uvula
Thinning and stiffening of the lips
Pigmentation of the oral mucosa
Dryness of the mouth and burning sensation (stomatopyrosis)
Decreased mouth opening and tongue protrusion

Causes
Dried products such as paan masala and gutkha have higher concentrations of areca nut and appear to cause the disease.
There is no specific antidote to barbiturate overdose; treatment is supportive, generally  including the administration of intravenous saline, naloxone, thiamine, glucose, sodium bicarbonate to alkalize the urine and increase rate of excretion, and activated charcoal via nasogastric tube.Acetaminophen exerts its toxicity through the production of a toxic metabolite that can cause liver damage at doses as low as four grams. Larger doses can precipitate acute liver failure, acute kidney injury, or gastrointestinal bleeding; death has been known to occur with ingestion of ten to fifteen grams. The specific antidote to acetaminophen overdose is N-acetylcysteine. Mechanism of action
Butalbital exerts a generalized depressant effect on the central nervous system and, in very high doses, has peripheral effects. Acetaminophen has analgesic and antipyretic effects mediated by a metabolite that acts at cannabinoid receptors. Caffeine is thought to produce constriction of cerebral blood vessels and serves to counteract the sedative effect of butalbital.Butalbital has a half-life of about 35 hours. Acetaminophen has a half-life of about 1.25 to 3 hours, but may be increased by liver damage and after an overdose. Caffeine has a half-life of about 2.5 to 4.5 hours. References
External links
"Acetaminophen mixture with butalbital". Drug Information Portal. U.S. National Library of Medicine. "Acetaminophen mixture with butalbital and caffeine". Drug Information Portal. U.S. National Library of Medicine.