Final answer:
The prolonged effects of succinylcholine are increased by a genetic condition known as pseudocholinesterase deficiency, which slows down the metabolism and excretion of the drug.
Step-by-step explanation:
The factor that contributes to an increased incidence of prolonged effects of succinylcholine is the incidence of pseudocholinesterase deficiency. Pseudocholinesterase is an enzyme necessary for the metabolism and excretion of succinylcholine. A deficiency in this enzyme leads to a prolonged duration of action of the drug because it cannot be broken down as quickly. This means that patients with this genetic condition will have longer-lasting paralysis, which is an intended effect of succinylcholine when used as a muscle relaxant during surgery.
Succinylcholine acts by inactivating the enzyme acetylcholinesterase, thus preventing the breakdown of the neurotransmitter acetylcholine. In individuals with pseudocholinesterase deficiency, their ability to break down succinylcholine is impaired, leading to prolonged neuromuscular blockade. Genetic illnesses related to metabolic deficiencies could potentially be managed by treatments that enhance or inhibit the activity of the specific enzyme involved, but in the case of succinylcholine and pseudocholinesterase, treatment options are limited and focus mainly on the awareness and identification of individuals with the deficiency.