Anaphylactic Shock Treatments Quiz

Adrenaline primarily acts on the heart through its interaction with the beta-2 receptors.

The vasoconstriction effect of high doses of adrenaline is mainly mediated by alpha-2 receptors.

Epinephrine's effect on bronchial muscles is relaxation, primarily mediated by alpha-2 receptors.

Adrenaline causes relaxation of smooth muscles in the gastrointestinal tract, primarily through beta-2 receptors.

Alpha-1 receptors are mainly present in the heart and kidneys.

Beta-2 receptors play a role in the contraction of the iris radial muscle, leading to mydriasis.

Acetylcholine primarily affects beta receptors on blood vessels.

Epinephrine is rapidly inactivated in the liver by Monoamine Oxidase (MAO) and Catechol-o-methyltransferase (COMT).

Norepinephrine has significant effects on beta-2 receptors.

Noradrenaline is used as a vasopressor agent in treating hypotensive states.

Propranolol increases heart rate.

Atropine is an adrenergic antagonist.

Norepinephrine causes vasodilation.

Acetylcholine is metabolized by MAO and COMT enzymes.

Epinephrine is ineffective when administered orally.

Propranolol can be used for the prophylaxis of angina pectoris.

Acetylcholine is a non-selective muscarinic and nicotinic agonist.

Atropine is a non-selective muscarinic antagonist.

Acetylcholine causes vasodilation through the NO pathway on vascular endothelium.

Adrenaline is commonly used as a cholinergic agonist in clinical practice.

Propranolol acts as a cholinergic antagonist.

Noradrenaline mediates its effects through activation of muscarinic receptors.