Radioactive iodine treatment is the therapy of choice in patients with Graves' disease. The patient should be prepared:

Choice A reason: Warfarin does not primarily prevent platelet aggregation. It is an anticoagulant that inhibits the synthesis of vitamin K-dependent clotting factors, which are necessary for blood clot formation. Although it affects the clotting process, it does not have a direct impact on platelets.

Choice B reason: Heparin does not have a longer half-life compared to warfarin. In fact, heparin has a relatively short half-life, which allows for rapid adjustments in dosing. This characteristic makes it suitable for acute management of conditions like deep vein thrombosis (DVT), where immediate anticoagulation is necessary.

Choice C reason: Heparin does not necessarily have fewer adverse effects compared to warfarin. Both medications have potential side effects and risks. Heparin can cause bleeding, heparin-induced thrombocytopenia (HIT), and other complications, while warfarin also carries a risk of bleeding and requires careful monitoring due to its interactions with foods and other medications.

Choice D reason: The onset of warfarin is slower than heparin. Heparin works rapidly to anticoagulate the blood and is often used for immediate management of conditions like DVT. Warfarin, on the other hand, takes several days to reach its full anticoagulant effect as it gradually reduces the levels of clotting factors. Therefore, patients are typically started on heparin for immediate effect and then transitioned to warfarin for long-term anticoagulation.

Choice A reason: Hyperbilirubinemia and jaundice are common manifestations of chronic liver disease, but they are not the primary cause of hepatic encephalopathy. These conditions result from the liver's inability to process and clear bilirubin effectively, leading to its accumulation in the blood and subsequent yellowing of the skin and eyes. While these symptoms indicate liver dysfunction, they do not directly cause the neurological impairments seen in hepatic encephalopathy.

Choice B reason: Fluid and electrolyte imbalances are often associated with chronic liver disease and can contribute to various complications, including ascites and edema. However, these imbalances are not the primary cause of hepatic encephalopathy. While electrolyte disturbances, particularly hyponatremia, can exacerbate encephalopathy, the condition itself is more directly linked to the liver's inability to detoxify certain substances, such as ammonia.

Choice C reason: Decreased cerebral blood flow can lead to neurological impairments, but it is not the primary mechanism underlying hepatic encephalopathy. Hepatic encephalopathy primarily results from the accumulation of neurotoxic substances that the liver can no longer effectively process, rather than reduced blood flow to the brain.

Choice D reason: Impaired ammonia metabolism and increased ammonia levels in the blood are the main causes of hepatic encephalopathy. In chronic liver disease, the liver's ability to convert ammonia, a byproduct of protein metabolism, into urea for excretion is compromised. As a result, ammonia accumulates in the blood and crosses the blood-brain barrier, leading to neurotoxicity and the characteristic symptoms of hepatic encephalopathy, such as confusion, altered consciousness, and asterixis (flapping tremor).