Delirium Tremens Flashcards
Q: What are the key pathophysiological mechanisms behind delirium tremens?
A: Delirium tremens results from a rebound hyperexcitability of the central nervous system due to the downregulation of GABA receptors and upregulation of NMDA receptors after chronic alcohol use, leading to a hyperadrenergic state when alcohol is withdrawn.
Q: What is delirium tremens (DT), and when does it typically occur?
A: Delirium tremens is a severe form of alcohol withdrawal characterized by confusion, agitation, hallucinations, and autonomic hyperactivity. It typically occurs 48-72 hours after the last alcohol intake.
Q: What are the main clinical features of delirium tremens?
A: Clinical features include severe agitation, tremors, hallucinations (visual, auditory, or tactile), confusion, disorientation, fever, tachycardia, hypertension, and diaphoresis.
Q: What are the risk factors for developing delirium tremens?
A: Risk factors include a history of heavy, prolonged alcohol use, previous episodes of DTs, older age, concurrent medical illness, and lack of timely intervention during alcohol withdrawal.
Q: What is the first-line treatment for delirium tremens?
A: The first-line treatment for delirium tremens is benzodiazepines, such as diazepam or lorazepam, which enhance GABAergic activity and help control agitation and prevent seizures.
Q: Why is thiamine administered to patients with delirium tremens?
A: Thiamine is administered to prevent Wernicke’s encephalopathy, a potentially life-threatening complication of alcohol use disorder characterized by confusion, ophthalmoplegia, and ataxia due to thiamine deficiency.
Q: Which parts of the brain are most affected in delirium tremens, and how do these areas contribute to the symptoms?
A: Delirium tremens primarily affects the cerebral cortex and limbic system. The disruption in GABAergic and glutamatergic neurotransmission leads to hyperexcitability in the cerebral cortex, causing agitation, confusion, and seizures. The involvement of the limbic system contributes to emotional instability, anxiety, and hallucinations. Additionally, autonomic centers in the hypothalamus are affected, leading to the autonomic hyperactivity seen in DTs (e.g., tachycardia, hypertension, hyperthermia).
