Seizures and Antiepileptic Therapy Quiz

Understanding Seizures and Antiepileptic Therapy

• Seizures are caused by abnormally excitable neurons firing in synchronization, influenced by potassium, calcium, sodium, and chloride channels in the neuronal membrane.
• Anti-epileptic agents target these channels to prevent firing, while upregulation of Synaptic Vesicle protein 2A (SV2A) is also linked to epilepsy.
• Drug and non-drug causes of seizures include premature birth, perinatal injury, alcohol withdrawal, febrile seizures, family history, stroke, head trauma, and infections.
• Known triggers for seizures include stress, photostimulation, hyperventilation, sleep deprivation, and hormonal changes.
• Antiepileptic therapy aims to prevent seizure recurrence and minimize side effects, and can be discontinued after 2-4 years of achieving seizure freedom.
• Seizure threshold describes the risk of experiencing a seizure, while the postictal period follows a seizure with altered consciousness or behavior.
• Focal (partial) seizures originate from a neural network in only one side of the brain and can have motor and/or non-motor components.
• Various antiepileptic drugs have different properties and mechanisms of action, including enzyme-inducing and non-enzyme-inducing drugs.
• Barbiturates such as phenobarbital and primidone have chronic side effects like behavioral and cognitive problems, mood changes, and sedation.
• Benzodiazepines like clobazam can lead to chronic side effects like depression, and tolerance may develop.
• Different antiepileptic drugs have idiosyncratic side effects and affect metabolic pathways, with implications for drug interactions and efficacy.
• Understanding the properties of antiepileptic drugs is crucial for optimizing therapy and managing side effects in individuals with seizures.

Gout Treatment and Urate-Lowering Therapies

• NSAIDs (indomethacin, naproxen, ibuprofen) are commonly used to treat gout attacks, but their efficacy decreases over time.
• Colchicine, when added to NSAIDs, can be used up to 24 hours from the onset of an acute gout attack, and up to 2-3 days after gout symptoms resolve.
• Colchicine mitigates the inflammatory response by neutrophils that contribute to gout symptoms, with primarily GI side effects.
• A 2019 trial demonstrated that colchicine was effective in the secondary prevention of major cardiac events after a myocardial infarction.
• Corticosteroids (oral, intra-articular, or intramuscular) have equal or superior efficacy to NSAIDs and colchicine, with no greater risks of adverse effects in most patients.
• Allopurinol is the first-line and mainstay of treatment for gout, with specific indications for starting urate-lowering therapy (ULT).
• ULT can be initiated during a gout attack for specific patient characteristics, and patients are advised to use colchicine or low-dose NSAIDs for at least 6 months after achieving target serum urate and no tophi on exam.
• During the first 6 months of ULT initiation, patients are most at risk for recurrent gout flares.
• The text includes references to several resources and guidelines on gout management and urate-lowering therapies.
• The use of ULT is discussed in the context of preventing gout flares and achieving target serum urate levels.
• The text emphasizes the importance of considering patient characteristics and specific indications when starting ULT.
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