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Ioedema, each hereditary and idiopathic. OCPs and ACE-I work on separate pathways in the pathogenesis of angioedema. We believe that the addition of a second medication that could influence the pathway that leads to angioedema was the trigger resulting in AIAI. AIAI is really a diagnosis established by exclusion. It should be suspected inside a patient on an ACE-inhibitor with distinct findings noted on imaging. The findings on CT abdomen inside the suitable clinical setting include ascites, little bowel wall thickening, dilatation, mesenteric edema and also a "donut" look. The diagnosis is established by resolution of symptoms following cessation from the ACE-inhibitor. AIAI can take place following months to years of becoming on an ACE-I. This situation typically goes unrecognized for quite a few years and causes significant emotional and financial trauma to the patient. The awareness of AIAI is essential amongst clinicians provided the higher frequency of use of ACE-I in individuals, delays in generating diagnosis and higher costs endured by the health care system as a result of this. Further, dysfunction of alternate diagnosis coupled with conservative and economical therapy make the understanding of AIAI an indispensible tool for physicians. A PECULIAR PRESENTATION OF PAINLESS PRINZMETAL'S ANGINA Naveen Nannapaneni. Wayne State University, Royal Oak, MI. (Tracking ID #2190203) Mastering OBJECTIVE #1: Recognize an atypical presentation of Prinzmetal's Angina. Learning OBJECTIVE #2: Distinguish Prinzmetal's Angina from myocardial infarction. CASE: A 48-year-old female with recurrent ovarian cancer, hypertension, as well as a history of mitral-valve replacement secondary to rheumatic fever presented for the ER with a 2-week complaint of intractable nausea, vomiting, and anorexia right after her most recent round of chemotherapy. She reports obtaining associated epigastric 23977191 23977191 fullness with no bowel movement or flatus for around four days. On initial evaluation she was found to be hypotensive and borderline tachycardic. Physical examination exhibited dry oral mucosa, a mechanical heart sound radiating towards the left axilla and diminished bowel sounds. Laboratory investigations revealed hyperkalemia, 6.5mMol/L, and an acute kidney injury, creatinine two.45 mg/dL. Abdominal x-ray showed a high grade proximal small-bowel obstruction. Initial EKG showed sinus tachycardia with no 23727046 23727046 hyperkalemic alterations. Hyperkalemia was treated with calcium gluconate, insulin and dextrose with gradual improvement. Serial EKGs revealed new J-point ST-segment elevations within the inferolateral leads with reciprocal alterations. Cardiology was consulted for a possible STEMI, bedside echocardiogram revealed no wall motion abnormalities and serial troponins had been negative even though the patient had no chest pain. Coronary angiography revealed only mild luminal irregularities as well as the patient was began on 773 Duchess Milford Mi isosorbide dinitrate for suspected coronary vasospasm. She underwent an exploratory laparotomy with lysis of adhesions, jejunostomy and feedingtube placement for management of her tiny bowel obstruction. Her all round clinical situation subsequent to the surgery progressively deteriorated as a result of sepsis, top to multi-organ failure and her eventual passing in palliative care soon after a month-long hospitalization. DISCUSSION: The typical presentation of Prinzmetal's Angina includes episodic anginal chest discomfort and ST-segment EKG adjustments suggestive of infarction with out fixed obstruction on coronary angiography that is as an alternative attributed to coronary vasospa.