Step 1: Read the question as a cholinergic or anticholinergic problem:
A muscarinic toxin from a mushroom acts like acetylcholine on muscarinic receptors. So the picture is the same as parasympathetic overactivity.
A simple way to think about it: muscarine pushes the rest and digest system as hard as possible.
Step 2: Use the memory aid for the cholinergic syndrome:
The common aid is SLUDGE (salivation, lacrimation, urination, defecation, gastric upset, emesis) and the 'killer B's': bradycardia, bronchorrhoea and bronchospasm.
Notice that heart rate falls in this list. Pupils are small, and the bladder empties easily.
Step 3: Look at the mechanism in the heart:
The SA node has M2 receptors. When they are stimulated, potassium channels open and the pacemaker potential rises more slowly.
This slows the heart, so bradycardia is expected.
Step 4: Test each option with the opposite syndrome:
Tachycardia, mydriasis and urinary retention are the classic features of atropine poisoning (the anticholinergic syndrome: 'hot as a hare, blind as a bat, dry as a bone, red as a beet, mad as a hatter').
All three are the reverse of what muscarine does. So options (A), (B) and (D) are wrong.
Step 5: Link to treatment:
Atropine is the specific antidote for muscarinic mushroom poisoning. It reverses bradycardia and the secretions.
The fact that the antidote itself causes tachycardia, mydriasis and urinary retention confirms that these three are not part of the toxin's action.
Final Answer:
Bradycardia is the expected clinical feature. This is option (C).