**Core Concept**
Competitive neuromuscular blockade is achieved through the inhibition of nicotinic acetylcholine receptors at the neuromuscular junction. This class of drugs, exemplified by rocuronium and vecuronium, competes with acetylcholine for receptor binding sites, thereby preventing muscle contraction.

**Why the Correct Answer is Right**
To reverse the effects of a competitive neuromuscular blocker, a drug that can outcompete the existing antagonist for receptor binding is required. Neostigmine, a cholinesterase inhibitor, increases the concentration of acetylcholine available for receptor binding, effectively displacing the antagonist and restoring neuromuscular transmission. This is achieved through the inhibition of acetylcholinesterase, the enzyme responsible for the breakdown of acetylcholine.

**Why Each Wrong Option is Incorrect**
**Option A:** This option is incorrect because anticholinergic drugs, such as atropine, would actually worsen neuromuscular blockade by further reducing acetylcholine availability.
**Option B:** Muscle relaxants like succinylcholine are depolarizing agents that would exacerbate neuromuscular blockade, rather than reverse it.
**Option C:** Steroids, such as dexamethasone, have anti-inflammatory properties but do not directly reverse neuromuscular blockade.

**Clinical Pearl / High-Yield Fact**
In patients with suspected or confirmed myasthenia gravis, the use of non-depolarizing neuromuscular blockers should be avoided due to the risk of worsening respiratory muscle weakness.

**Correct Answer: D. Neostigmine. This drug can be administered to reverse the effects of a competitive neuromuscular blockade.**