United States Medical Licensing Examination (Step One)

Adriamycin, also known as doxorubicin, is a chemotherapeutic agent commonly used in the treatment of various cancers, including non-Hodgkin's lymphoma. One of the most significant and well-documented adverse effects of adriamycin is cardiomyopathy, which can lead to congestive heart failure. The patient's symptoms of progressive shortness of breath, fatigue, jugular venous distension, and bilateral lower extremity edema, along with a reduced ejection fraction on echocardiogram, are classic signs of heart failure. Given the temporal relationship between the completion of chemotherapy and the onset of symptoms, adriamycin-induced cardiomyopathy is the most likely diagnosis. This condition occurs due to the cumulative dose-dependent cardiotoxicity of adriamycin, which leads to myocardial cell damage and subsequent heart failure.

Hypertension is not the most likely adverse effect of adriamycin on the cardiovascular system in this context. While hypertension can cause symptoms of heart failure, it is not a common side effect of adriamycin. Bradycardia, or a slow heart rate, is also not typically associated with adriamycin use. Myocardial infarction, or heart attack, presents with different symptoms such as chest pain and is not directly linked to adriamycin toxicity. Pulmonary embolism, a blockage in the pulmonary arteries, would present with acute symptoms such as sudden shortness of breath and chest pain, and is not a known side effect of adriamycin. The patient's clinical presentation and recent chemotherapy with adriamycin strongly suggest cardiomyopathy as the most likely adverse effect.

The most likely cause of the patient's symptoms is atorvastatin. Statins, such as atorvastatin, are well-known to cause drug-induced myopathy, which can present as muscle pain, weakness, and elevated serum creatine kinase (CK) levels. The patient's history of hyperlipidemia and the use of atorvastatin, combined with his clinical presentation of muscle tenderness, reduced muscle strength in proximal muscles, and elevated CK levels, strongly suggest statin-induced myopathy. This adverse effect is dose-dependent and can occur months after initiating therapy, which aligns with the patient's timeline of symptom progression over the past 3 months.

Lisinopril is an angiotensin-converting enzyme (ACE) inhibitor used to treat hypertension. While it can cause side effects such as cough, hyperkalemia, and angioedema, it is not commonly associated with muscle weakness, pain, or elevated CK levels. Cocaine is a stimulant drug that can cause various cardiovascular and neurological effects, but it is not typically associated with the chronic muscle symptoms described in this patient. Vitamin D deficiency can lead to muscle weakness and pain, but it is less likely given the patient's medication history and the presence of elevated CK levels, which are more indicative of a drug-induced myopathy. Rheumatoid arthritis is an autoimmune condition that can cause joint pain and muscle weakness, but it would not typically present with elevated CK levels and is less likely given the patient's medication history and the absence of joint-specific symptoms.

The ACTH stimulation test is the most appropriate next step in confirming the diagnosis of Addison disease. This test evaluates the adrenal glands' ability to produce cortisol in response to synthetic ACTH. In Addison disease, the adrenal glands are damaged and cannot produce adequate cortisol, even when stimulated by ACTH. Therefore, a subnormal increase in cortisol levels after ACTH administration confirms the diagnosis. This test is highly specific and sensitive for primary adrenal insufficiency, making it the gold standard for diagnosing Addison disease.

Serum cortisol measurement alone is not the best diagnostic tool for Addison disease because cortisol levels can fluctuate throughout the day and may be influenced by stress or illness. While low cortisol levels can suggest adrenal insufficiency, they are not definitive without further testing. MRI of the adrenal glands can help identify structural abnormalities but is not necessary for the initial diagnosis and does not provide functional information about cortisol production. A 24-hour urine cortisol test measures cortisol excretion over a day and is more useful for diagnosing Cushing's syndrome rather than Addison disease. Complete blood count can provide supportive information, such as anemia or eosinophilia, but it is not specific for diagnosing adrenal insufficiency.

Drug-induced exanthematous eruption, also known as a morbilliform or maculopapular drug eruption, is the most likely diagnosis given the patient's history and clinical presentation. This type of eruption is a common adverse reaction to medications, particularly new ones, and typically presents as a widespread, symmetric, erythematous rash composed of macules and papules. The rash often starts on the trunk and spreads to other areas, which aligns with the patient's symptoms of a pruritic, erythematous rash on the chest and back. The absence of vesicles, pustules, and systemic symptoms such as fever further supports this diagnosis. The patient's recent initiation of a new antihypertensive medication is a key clue, as drug-induced exanthematous eruptions commonly occur within 1-2 weeks of starting a new drug.

Contact dermatitis is less likely because the patient denies any new exposures to soaps, lotions, or other potential allergens, and the rash is more widespread rather than localized to areas of direct contact. Psoriasis is characterized by well-demarcated, silvery-scaled plaques, typically on extensor surfaces, which does not match the description of the patient's rash. Lupus erythematosus often presents with a malar rash or discoid lesions, and systemic symptoms are usually present, neither of which are noted in this patient. Impetigo is a bacterial skin infection that presents with honey-colored crusts and pustules, which are not observed in this case.

Methotrexate is considered the first-line disease-modifying antirheumatic drug (DMARD) for the treatment of rheumatoid arthritis (RA) when patients do not respond adequately to NSAIDs and low-dose prednisone. Methotrexate works by inhibiting dihydrofolate reductase, leading to reduced DNA synthesis and cellular replication, which helps to control the inflammatory process in RA. It has been shown to be effective in reducing symptoms, improving physical function, and slowing the progression of joint damage. Additionally, methotrexate has a well-established safety profile and is generally well-tolerated when used at the doses prescribed for RA.

Aspirin, while an NSAID, is not typically used as a primary treatment for RA due to its limited efficacy in controlling the disease's progression and potential for gastrointestinal side effects. Azathioprine is an immunosuppressive agent that can be used in RA but is generally reserved for patients who do not respond to methotrexate or other first-line DMARDs due to its higher risk of adverse effects. Hydroxychloroquine is another DMARD that can be used in RA, but it is usually considered when methotrexate is contraindicated or as an adjunctive therapy rather than a primary treatment. Acetaminophen is an analgesic that can help manage pain but does not have anti-inflammatory properties or the ability to modify the disease course in RA.