Patient may have hereditary angioedema, which is associated with "recurrent attacks of intense, massive, localized subcutaneous edema involving the extremities, genitalia, face, or trunk, or submucosal edema of upper airway or bowels". The article goes on to say "C1-esterase inhibitor works directly on the complement and contact plasma cascades to reduce bradykinin release" which is also probably good to know.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3666183/

This patient has ACQUIRED ANGIOEDEMA, which is different from Hereditary. In Hereditary you do NOT present with urticaria as mentioned by some previous comments.

https://aacijournal.biomedcentral.com/articles/10.1186/1710-1492-6-14

Acquired angioedema (AAE) is characterized by acquired deficiency of C1 inhibitor (C1-INH), hyperactivation of the classical pathway of human complement and angioedema symptoms mediated by bradykinin released by inappropriate activation of the contact-kinin system.

seems this hereditary angioedema lacks well, everything that is hereditary angioedema. Thats some good family fun there eh Cotton

Hereditary angioedema (HAE) caused by C1-esterase inhibitor deficiency is an autosomal-dominant disease resulting from a mutation in the C1-inhibitor gene. HAE is characterized by recurrent attacks of intense, massive, localized subcutaneous edema involving the extremities, genitalia, face, or trunk, or submucosal edema of upper airway or bowels. Routine long-term prophylaxis with either attenuated androgens or C1-esterase inhibitor has been shown to reduce the frequency and severity of HAE attacks.

This is what I came across putting the two (angioedema + laryngospasm) together. Take into account that this info is regarding ACEIs but, I guess with a certain severity, angioedema can be associated with other sx. "However, angioedema has occurred suddenly after months to years of therapy, and about 20% of known cases of angioedema occurring in this context may involve severe symptoms (e.g., dyspnea, stridor, laryngospasm)."

https://www.sciencedirect.com/topics/medicine-and-dentistry/angioedema

I don't believe this question is addressing hereditary angioedema (which is definitely a manifestation of C1-INH deficiency), but rather just overactive complement (since its inhibitor is deficient). Remember that byproducts of the complement cascade include C3a, C4a, and C5a, which are all anaphylatoxins. "Episodes of cutaneous urticaria and occasional episodes of laryngospasm" describes an allergic reaction that can be mediated by the anaphylatoxins produced in the cascade. The other answer choices would lead to decreased complement activity and therefore release of fewer anaphylatoxins.