lesson 1.2

INSTRUCTIONS
1. You are to create a concept map based on the given case study. You can either use the electronic version available on Dabbleboard, another computerized concept map program, or you can draw your own. You may not copy one that is already done. Your submission must be your own original work.
2. Concept map requirements for inclusion:
a. Demonstrate the pathophysiological concepts that pertain to this case study.
b. Indicate relationships between concepts—group clusters or patterns of signs and symptoms.
3. Complete the critical thinking questions.
a. Demonstrate your understanding of the case by answering the critical thinking questions.
b. References should be in APA format.
CONCEPT MAP CASE STUDY ASSIGNMENT
Case:
57-year-old male with history of hypertension was just placed on lisinopril. He presents to the Emergency Department with a swollen uvula, difficulty breathing and swallowing.
PMHx: Hypertension, Type 2 Diabetes Mellitus (diet controlled), Obesity
Meds: Lisinopril 20 mg daily
Vitals: HR 90 BP 140/90 RR 24 Sat 96% RA Temp 37C
General: Nontoxic.
HEENT: Mild upper lip swelling, moderate uvula swelling but airway patent. No tongue swelling. No rash, erythema, or exudate.
Lungs: Clear throughout. No resp distress. CV: S1S2, no murmur, rub, or gallop.
Abd: Soft, nontender, nondistended.
Extrem: Warm, well perfused, without cyanosis or edema.
Neuro: Nonfocal.
Critical Thinking Questions:
1. What is the most appropriate treatment for this patient, and why?
2. What is the cross-reactivity risk if using an ACE Inhibitor Receptor Blocker in this patient, given this presentation? Explain the pathophysiology of this risk.
The overall incidence of angioedema in patients receiving ACE inhibitors is between 0.1 percent and 0.7 percent. ACE inhibitors are the most leading cause of drug-induced angioedema, responsible for up to 40 percent of emergency visits for angioedema. ACE inhibitor-induced angioedema usually affects the lips, tongue, and face, although visceral edema presenting as acute abdominal pain is also possible. Urticaria and itching are absent. Symptoms typically begin during the first week of treatment, although some cases develop after years of successful therapy.
Pathophysiology: The ACE inhibitors always blocks the outcome of the enzyme ACE, which is also known as kininase II, and affect the renin–angiotensin-aldosterone pathway (RAA) and the degradation of bradykinin. The RAA cascade is very important in regulating renal blood flow and blood pressure. Angiotensinogen, produced in the liver, is converted by renin in the kidney to produce angiotensin I. Angiotensin I is then metabolized to angiotensin II in the lungs by the enzyme ACE (kininase II). Angiotensin II acts as a vasoconstrictor through stimulation of angiotensin I and II receptors. Angiotensin II is also responsible for inactivating bradykinin while ACE (kininase II) is the primary peptidase involved in the degradation of bradykinin. Bradykinin is a peptide made of nine amino acids that increases capillary permeability and acts as a potent vasodilator. The production of bradykinin occurs after the precursor kininogen is cleaved by kallikrein which leads to production of the active form of bradykinin .
TREATMENT — The primary treatments of ACE inhibitor-induced angioedema are discontinuation of the drug and airway management if the mouth or throat is involved. Additional therapies may be helpful for severe or persistent symptoms.
Airway management — If the mouth or throat is involved, the airway should be immediately evaluated and repeatedly monitored until the swelling is clearly resolving. Prompt intubation and mechanical ventilation may be required.
Discontinue ACE inhibitor — Angioedema caused by ACE inhibitors usually resolves within 24 to 72 hours. If ACE inhibitors are continued, there is an increased and unpredictable rate of angioedema recurrence and attacks may become more severe or life threatening. Patients who have experienced angioedema attributed to an ACE inhibitor should never again be treated with this group of medications.
If the cause of a patient’s angioedema is unclear, we would still advise discontinuation of ACE inhibitors. If the patient experiences recurrent episodes of angioedema beyond four to six weeks, then the cause of the angioedema is likely not the ACE inhibitor and other etiologies should be explored. Other interventions — Antihistamines, glucocorticoids, and epinephrine are commonly used to treat allergic, histamine-induced angioedema. These medications are not known to alter levels of bradykinin and are usually considered ineffective or minimally effective in treating ACE inhibitor-induced angioedema. Despite this, a small number of studies have reported the apparent benefit with antihistamines in ACE inhibitor-induced angioedema

References:
Gelée B, Michel P, Haas R, Boishardy F. [Angiotensin-converting enzyme inhibitor-related angioedema: emergency treatment with complement C1 inhibitor concentrate]. Rev Med Interne 2008; 29:516.
Siragy HM. A current evaluation of the safety of angiotensin receptor blockers and direct renin inhibitors. Vasc Health Risk Manag 2011; 7:297.
Haymore BR, Yoon J, Mikita CP, et al. Risk of angioedema with angiotensin receptor blockers in patients with prior angioedema associated with angiotensin-converting enzyme inhibitors: a meta-analysis. Ann Allergy Asthma Immunol 2008; 101:495.
Beavers CJ, Dunn SP, Macaulay TE. The role of angiotensin receptor blockers in patients with angiotensin-converting enzyme inhibitor-induced angioedema. Ann Pharmacother 2011; 45:520.

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