ABEM Pharmacology & Medical Management Flashcards
6 cards from real ABEM practice questions. Tap to flip, then mark Knew It or Still Learning — missed cards come back until you master them.
Read the first 6 ABEM Pharmacology & Medical Management flashcards as text
Intravenous immunoglobulin (IVIG) is an effective treatment for Guillain-Barré syndrome primarily by:
Answer: Modulating the immune response and neutralizing pathogenic antibodies
IVIG works through multiple immune-modulating mechanisms including neutralizing pathogenic antibodies, blocking Fc receptors, and modulating complement activity.
Which class of drugs is contraindicated in myasthenia gravis due to risk of exacerbating neuromuscular transmission?
Answer: Beta-blockers and aminoglycoside antibiotics
Beta-blockers and aminoglycoside antibiotics can worsen neuromuscular transmission and precipitate myasthenic crisis.
Edaravone (Radicava) is FDA-approved for ALS and works primarily as:
Answer: A free radical scavenger (antioxidant)
Edaravone is a free radical scavenger that reduces oxidative stress, thought to contribute to motor neuron degeneration in ALS.
Gabapentin and pregabalin are frequently used for neuropathic pain because they bind to:
Answer: Alpha-2-delta subunit of voltage-gated calcium channels
Gabapentinoids bind to the alpha-2-delta subunit of voltage-gated calcium channels, reducing calcium influx and thereby decreasing neurotransmitter release from sensitized neurons.
Plasma exchange (plasmapheresis) is beneficial in Guillain-Barré syndrome primarily by:
Answer: Removing pathogenic antibodies and complement factors from circulation
Plasmapheresis physically removes circulating pathogenic antibodies, complement, and other humoral factors that attack peripheral nerve myelin in GBS.
Which metabolic condition, if untreated, leads to a neuropathy that can mimic hereditary motor and sensory neuropathy on NCS?
Answer: Refsum disease (phytanic acid accumulation)
Refsum disease causes accumulation of phytanic acid due to a deficient peroxisomal enzyme, resulting in a demyelinating polyneuropathy resembling HMSN on nerve conduction studies.