Autonomic pharmacology questions.

Answer: Vasoconstriction and dilation of the pupil

α₁ receptors sit on vascular smooth muscle and on the radial muscle of the iris, and in both places activation causes contraction. The consequence just looks different depending on the tissue: a contracted vessel narrows, while a contracted radial muscle widens the pupil.

Answer: β₂, found on bronchial smooth muscle

β₂ receptors relax bronchial smooth muscle, which is why salbutamol is a β₂ agonist and why non-selective beta blockade causes trouble in asthma. The pairing to remember is that β₁ is mostly cardiac and β₂ is mostly everything else smooth and relaxing.

Answer: Dry, flushed, hot, blind and confused

Atropine blocks muscarinic receptors, so every parasympathetic effector loses its input at once: glands stop secreting, so the patient is dry; sweating fails, so heat cannot be lost; the ciliary muscle cannot accommodate, so vision blurs. Central blockade adds the confusion.

Answer: Crosses the blood-brain barrier as a tertiary amine

Neostigmine carries a permanent positive charge as a quaternary ammonium compound, which keeps it out of the central nervous system. Physostigmine is uncharged at physiological pH, so it crosses, which is why it is used when central anticholinergic toxicity has to be reversed.

Answer: Atropine masks the symptoms; pralidoxime frees the enzyme

The two drugs treat different halves of the same problem. Atropine blocks the receptors that excess acetylcholine is flooding but does nothing to the cause. Pralidoxime prises the organophosphate off acetylcholinesterase, and must be given before ageing makes that bond permanent.

Answer: β₂ stimulation shifts potassium into cells

β₂ receptors are not confined to the airway. In skeletal muscle they produce tremor, and they also activate the Na⁺/K⁺-ATPase that pumps potassium into cells, lowering the plasma level without any potassium being lost from the body. Both are on-target effects in the wrong tissue.

Answer: Raised blood pressure triggers a baroreceptor response

Phenylephrine is a pure α₁ agonist and does nothing to the heart directly. The vasoconstriction it causes raises blood pressure, baroreceptors detect the rise, and vagal outflow slows the heart in compensation. The bradycardia is the body answering the drug, not the drug acting on the heart.

Answer: A fall in heart rate and slowed AV conduction

M₂ is the cardiac muscarinic receptor and it carries the vagal brake, slowing conduction through the SA and AV nodes. M₃ is the subtype that contracts smooth muscle and drives secretion, which is why the other options describe M₃ effects rather than M₂ ones.

Answer: Autonomic ganglia and the neuromuscular junction

Nicotinic receptors are ligand-gated ion channels used wherever a signal has to cross fast: at every autonomic ganglion, sympathetic and parasympathetic alike, and at the neuromuscular junction. Muscarinic receptors are G-protein coupled and sit at the slower effector end.

Answer: β₂ vasodilation predominates before α₁ effects appear

Adrenaline binds β₂ receptors with higher affinity than α₁, so at low concentrations the vasodilating effect in skeletal muscle beds appears first. As the dose climbs, α₁ vasoconstriction recruits and overwhelms it, which is why the same drug can lower or raise diastolic pressure.