Mechanisms of Self-Defense: Angioedema - Essay Example

"Mechanisms of Self-Defense: Angioedema" is an outstanding example of a paper on symptoms.
According to the symptoms presented, the patient is suffering from angioedema. This is an allergic-type reaction of medication; thus the mid-upper lip swelling. This reveals that the patient is allergic to lisinopril. In addition, the patient has difficulty in breathing and swallowing, an outcome of the moderate swelling of the uvula. To be more specific to this diagnosis, the patient is suffering from angiotensin-converting enzyme (ACE) inhibitor angioedema (McCance & Huether, 2014 p. 262).

The aptest treatment for this patient is immediate intubation and mechanical ventilation as the airway is rapidly swelling and compromised. According to this case, ventilation is threatened by swelling of the uvula. Recommendations for this treatment include 12- 24 hours of critical observation and hospitalization. Monitoring is vital as this is a life-threatening condition and may lead to respiratory arrest and even death. In addition, the halt of lisinopril and other medication is taken by the patient is advised as a treatment action; in determining the cause of the reaction. Medication, which must be administered to the patient, includes the administration of antihistamines, epinephrine, H-2 blockers, corticosteroids, and androgens. As soon as the swelling has subsided, no further treatment is necessary; rather than avoidance of the drug (lisinopril and other ACE medication) that triggered the reaction. Research conducted by Karim & Masood (2002) revealed an alternative treatment for ACE induced angioedema by the introduction of fresh frozen plasma. This is because the fresh frozen plasma supplies a chemical that is identical to the angiotensin-converting enzyme and breaks down the excess bradykinin (p. 370-371).

Cross-reactivity risk of using an ACE Inhibitor Receptor Blocker in this patient

Several studies have revealed that there is cross-reactivity between ACE inhibitors and Angiotensin receptor blocker (ARB). There is an irregularity of cross-reactivity for angioedema with Angiotensin receptor blockers (ARB), an ACE inhibitor receptor blockers that have an effect on the Rennin Angiotensin Aldosterone System. ACE inhibitors block the working of the enzyme ACE. This enzyme is liable for the breakdown of bradykinin, lack of its breakdown results to an increase in the peripheral tissues (Koda-Kimble & Alldredge, 2013 p. 464).

ACE inhibitors and ARBs impede with angiotensin II through receptor inhibition or decreased production. Angiotensin II acts as the activator of bradykinin its inhibition contributes to drastic outcomes. This is the destruction of the peptide bradykinin, which causes vasodilation. Blocking of the ACE inhibitors will directly, or indirectly decrease the level of angiotensin II development, leading to angioedema, hypotension, acute renal failure, cough anaphylactic reactions, and hyperkalemia (Brashers, 2006).

There is a cross-reactivity risk of using an ACE inhibitor receptor blocker in this patient as it may lead to adverse complications and even death.  Therefore, the use of ACE receptor blockers should be used with care as the patient has experienced ACE inhibitor triggered angioedema. Justification for the use of these blockers is necessary for the treatment of heart failure, hypertension, and chronic kidney disease. This based on the fact that the mechanism of the ACE inhibitor will be blocked, noting that the patient is undergoing an anaphylactic response.