Medical Knowledge 9 Flashcards

A patient on long-term linezolid for a resistant infection is prescribed tramadol for post-procedural pain. Within 3 hours he develops agitation, hyperthermia (39.8°C), and prominent clonus with hyperreflexia. Which single finding most reliably distinguishes this presentation from Neuroleptic Malignant Syndrome (NMS)?

Answer: Presence of clonus and hyperreflexia

Clonus and hyperreflexia are hallmark features of serotonin syndrome caused by excess serotonergic activity. Linezolid has weak MAO-inhibiting properties, and tramadol inhibits serotonin reuptake — a dangerous combination. NMS, caused by dopamine blockade, presents with 'lead-pipe' muscular rigidity and bradyreflexia, NOT clonus. While elevated CK, hyperthermia, and rapid onset can occur in both conditions, only the neuromuscular pattern (hyperreflexia/clonus vs. rigidity/bradyreflexia) reliably differentiates them.

A 58-year-old man presents to the ED with chest pain that fully resolved 8 hours ago. Current ECG shows deeply symmetric T-wave inversions in leads V2–V3 with no ST elevation. Troponin is mildly elevated. He is hemodynamically stable. What is the most appropriate next step?

Answer: Refer for urgent cardiac catheterization

This presentation is classic for Wellens Syndrome Type B (deep symmetric T-wave inversions in V2–V3), which is a pre-infarction pattern indicating critical proximal left anterior descending (LAD) artery stenosis. These patients are at extreme risk for massive anterior MI. Exercise stress testing is absolutely contraindicated — it can precipitate complete occlusion. Thrombolytics are inappropriate without ST elevation or occlusion confirmed. Urgent angiography with revascularization is the correct management.

A patient stabilized on lithium (level 0.9 mEq/L) for bipolar I disorder is started on ibuprofen by his GP for knee osteoarthritis. Three days later he presents with coarse tremor, confusion, and ataxia. Repeat lithium level is 2.1 mEq/L. What is the pharmacological mechanism of this interaction?

Answer: Ibuprofen inhibits renal prostaglandin synthesis, reducing GFR and decreasing lithium clearance

Lithium is excreted almost entirely unchanged by the kidneys and is NOT protein-bound or hepatically metabolized. NSAIDs like ibuprofen inhibit prostaglandin synthesis, which reduces afferent arteriolar dilation and decreases glomerular filtration rate (GFR). Since lithium clearance is directly proportional to GFR, reduced GFR leads to lithium accumulation and toxicity. This interaction is clinically significant and potentially life-threatening — NSAIDs should be avoided in lithium-treated patients.

A patient with subarachnoid hemorrhage (SAH) on day 4 develops serum sodium of 122 mEq/L, serum osmolality of 258 mOsm/kg, and urine sodium of 85 mEq/L. Clinical examination reveals dry mucous membranes, decreased skin turgor, and orthostatic hypotension. What is the correct diagnosis and management?

Answer: Cerebral salt wasting — treat with isotonic or hypertonic saline plus volume replacement

The clinical picture is Cerebral Salt Wasting (CSW), not SIADH. Both present with hyponatremia and elevated urine sodium in the context of brain injury, making differentiation critical. The key distinguishing feature is volume status: SIADH is euvolemic or mildly hypervolemic, while CSW is hypovolemic (as evidenced here by dry mucous membranes and orthostatic hypotension). Treating CSW with fluid restriction (as for SIADH) would be catastrophically dangerous in SAH, worsening vasospasm and cerebral ischemia. CSW requires volume replacement with saline.

A 42-year-old woman with known but untreated Graves' disease undergoes emergency appendectomy. Six hours post-operatively she develops temperature 40.4°C, heart rate 152 bpm with atrial fibrillation, and moderate confusion (Burch-Wartofsky score >45). Regarding the correct sequence of medication administration, which order is most important?

Answer: Propylthiouracil (PTU) → then potassium iodide at least one hour later

In thyroid storm, a thionamide (PTU preferred over methimazole as it also blocks peripheral T4-to-T3 conversion) MUST be administered before iodine. If iodine is given first, it provides additional substrate for thyroid hormone synthesis — the 'Jod-Basedow effect' — paradoxically worsening the storm. PTU/methimazole first blocks new hormone synthesis and organification; only then does iodine administration reduce thyroid vascularity and inhibit hormone release safely. Radioactive iodine is absolutely contraindicated in thyroid storm.

A 54-year-old woman taking hydralazine for hypertension for 22 months develops pleuritis, malar rash, and arthralgia. Labs show positive ANA (titer 1:640), positive anti-histone antibodies, negative anti-dsDNA antibodies, and serum creatinine 0.9 mg/dL. What finding regarding complement levels distinguishes this diagnosis from idiopathic systemic lupus erythematosus (SLE)?

Answer: Normal C3 and C4 complement levels

Drug-induced lupus (DIL) caused by hydralazine characteristically presents with normal complement (C3 and C4) levels, in contrast to idiopathic SLE which typically shows hypocomplementemia due to immune complex-mediated complement consumption. The antibody profile also differs: DIL is characterized by anti-histone antibodies and negative anti-dsDNA, while idiopathic SLE commonly features anti-dsDNA and anti-Smith antibodies. Additionally, DIL rarely causes serious renal involvement. Recognizing this distinction prevents misclassification and guides management — stopping hydralazine typically leads to resolution.