If a cell has two different GPCRs, how does the cell differentiate between the phosphorylation cascade caused by each?
First, it would be an oversimplification to say that GPCRs act only through increases in cytosolic cAMP. This is true for receptors coupled to Gs proteins, but there are other G proteins like Gi, Go and Gq which act differently [1]. 

Now, a cell can have receptors coupled to many different G proteins. Vascular smooth muscle, for instance, has Gs, Gi and Gq-coupled receptors [2]. Further, a cell can have different receptors coupling to G proteins of the same type (e.g., hepatocytes have glucagon and beta adrenergic receptors [3], which both couple to Gs).

In such situations, the effects of different hormones add up. The final effect is a function of the total cytosolic concentration of second messenger (e.g., cAMP). Thus glycogen breakdown in a hepatocyte depends on the overall effects of glucagon and epinephrine [3]. The hepatocyte has no way of 'knowing' which cAMP molecule was formed by which hormone.

References


https://en.wikipedia.org/wiki/Heterotrimeric_G_protein
https://cvphysiology.com/Blood%20Pressure/BP026
https://www.nature.com/articles/emm2015122