2017 Final Booklet

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2017 Final Booklet Illinois Chapter Northern Region Top 100 Posters University of Illinois at Chicago November 8, 2017 Last Name: Abaribe First Author: Resident First Name: Obinna Category: Clinical Vignette ACP Member: 3363118 Additional Authors: Bibek Pannu Title: Loperamide Poor man’s methadone related Cardiotoxicity Abstract: There is recent emerging trend to use over the counter Loperamide at higher doses for euphoric effects. There is a growing demand amongst educated people and loperamide appears to fit that role. At higher doses loperamide crosses the blood brain barrier and produces euphoric effects Euphoric effect starts around 300- 400 mg per day as compared to recommended dose of 5-10 mg per. As per poison control data there is recent surge in the number of cases in iIlinois. A 32 –year old male patient with history of Substance use, scoliosis and back surgery presented to ED via ambulance after a witnessed seizure like activity and acute confusion. The Patient has been taking 100 to 200 capsules of loperamide Every other day. At Presentation, He appeared distressed but was oriented to person place and time. He reported no Bowel movement for three days, palpitations, fatigue and chills. Examination of Vitals, chest scan, cardiovascular examination, and abdominal palpitations were without incidence. He was noted to have prolonged QT of 634, several episodes of Vtach and Afib on EKG and Telemonitor. He received magnesium, lidocaine infusion, isoproterenol, and Bicarb. Cardioversion was done by Electrophisiology with Brief conversion to sinus rhythm. The Patient was taken to cath lab for placement of a temporary pace maker. A 2D Echo was done which showed Normal left ventricular systolic and diastolic function with dyskinetic inter ventricular septal motion due to pacemaker or LBBB. CT and MRI of the brain were unremarkable. Patients often combine other medications in an attempt to increase loperamide absorption and penetration across the blood-brain barrier, inhibit its metabolism, and enhance its euphoric effects. If toxicity is suspected, the drug should be promptly discontinued and necessary therapy begun; if loperamide ingestion is suspected, blood levels should be measured, which may require specific testing. For cases of torsades de pointes in which drug treatment is ineffective, electrical pacing or cardioversion may be required. 1. Raminta Daniulaityte, Robert Carlson, Russel Falck, et al I Just Wanted to Tell You That Loperamide WILL WORK”: A Web-Based Study of Extra-Medical Use of Loperamide. Drug Alcohol Depend. 2013 Jun 1; 130(0): 241–244. Published online 2012 Nov 30 2 Venosa, Ali. "Opiate Withdrawal Driving People to Abuse Diarrhea Medication Imodium: Overdoses Causing Cardiac Dysrhythmia, Death." 4 May 2016. Medical Daily. 5 May 2016. http://www.medicaldaily.com/opiate-withdrawal-diarrhea-medication-imodium-cardiac- dysrhythmia-384700 Last Name: Abbasi First Author: Resident First Name: Taimur Category: Clinical Vignette ACP Member: 3040185 Additional Authors: Thomas Joseph, MD; Gaurav K. Sharma, MD. Title: Allergic Myocardial Infarction: A case of Kounis with Samter’s Syndrome. Abstract: Introduction: Kounis syndrome (KS) has been described as an allergic insult leading to hypersensitivity reaction culminating in the occurrence of an acute coronary event. This recently identified entity has primarily been described as a dynamic vasospastic event that is mediated by mast cell degranulation. Below we present a case where aspirin allergy led to an allergic myocardial event. Case Description: A 63-year-old man presented with chest pain (CP) and urticaria. History was significant for, asthma, nasal polyps, sinusitis and multiple episodes of CP with a negative angiographic workup. Multiple drug allergies, which resulted in urticaria and dyspnea. Past episodes of CP and urticaria were relieved by nitroglycerin (NTG). Cardiac catheterization (CC) showed patent coronaries, but was conspicuous for coronary artery spasm (CAS), that was relieved by intracoronary NTG (IC-NTG). Patient was placed on aspirin (ASA), calcium channel blocker (CCB), statin, nitrate and ranolazine. A few weeks’ later patient presents with repeat onset of CP, dyspnea and urticaria. He is treated for a non-ST segment elevation myocardial infarction (NSTEMI) and undergoes CC that shows subtotal occlusion of a coronary. Failed trial of IC-NTG was followed by stent deployment resulting in resolution of occlusion. Patient was restarted on ASA and clopidogrel. Following day, patient again complains of severe CP, ECG shows ST segment elevation myocardial infarction (STEMI) accompanied by troponemia. Patient undergoes a repeat CC that shows patent coronaries and stent. Furthermore, there is spontaneous resolution of ECG changes. At this juncture, an immune mediated etiology to symptoms is suspected.ASA is stopped and a different platelet inhibitor is started. Patient is evaluated by an immunologist and is diagnosed with Samter-Beer syndrome characterized by asthma, nasal polyposis and ASA allergy. Patient is started on a histamine antagonist and ASA desensitization. In the following months’ patient is admitted twice with symptoms of CP and urticaria, ECG changes consistent with STEMI and troponemia. CC in both episodes shows CAS that is treated with IC-NTG. Similar to all prior instances, CC showed angiographically patent stent and preserved cardiac function. All episodes of CP were accompanied by urticaria mostly confined to the lower extremities. At this juncture the patient is diagnosed with KS. Patient was started on intense antihistamine therapy, coronary antispasmodics and discharged home with complete resolution of symptoms. Discussion: Based on the presence or absence of preexisting coronary disease, KS is classified into different variants. Precipitants include foods, insect stings, and various drugs. Treatment consists of revascularization, control of anaphylaxis and supportive therapy. This entails the use of antihistamines, steroids, epinephrine and mast cell stabilization. Last Name: Abraham First Author: Resident First Name: Hrudya Category: Clinical Vignette ACP Member: 3054207 Additional Authors: Jacqueline R Chua MD, Padmanabhan Raghu MD Title: Dysphagia in Dermatomyositis : A Forerunner of Cancer Abstract: Background Dermatomyositis (DM) can be associated with dysphagia and various internal malignancies. Dysphagia has been reported due to skeletal muscle involvement in DM but is more frequent in patients with internal malignancy. DM is rarely associated with esophageal cancer as described in our patient below. Hence it is critical to differentiate the dysphagia secondary to malignancy from that of DM. Case Description A 59 –year- old female with past medical history of diabetes and hypertension presented to our clinic for evaluation of progressively worsening rash for 2 months. The rash started underneath her eyes spreading to her face, chest, back, arms and her hands. On exam, erythematous scaly lesions were seen in the above-mentioned areas in addition to proximal muscle weakness. Labs were significant for microcytic anemia, elevated aldolase and creatinine kinase (CK). Skin biopsy and EMG were consistent with diagnosis of DM. She was started on prednisone, mycophenolate and hydroxychloroquine with improvement in skin lesions. Four months after initial diagnosis of DM, she developed progressive dysphagia to solids and liquids with worsening skin lesions and muscle weakness. On exam she had oral thrush in addition to rash and proximal myopathy. Upper endoscopy showed ulcerating mass, biopsy of which showed poorly differentiated adenocarcinoma with presence of Helicobacter. Discussion DM is an inflammatory myopathy characterized by symmetrical progressive muscle weakness, characteristic skin rash, elevated CK, abnormal EMG and muscle biopsy. It is known to be associated with malignancy and the reported incidence varies between 7 to 34%. It usually precedes lung, breast, nasopharyngeal and ovarian malignancies even-though less commonly associated with esophageal cancer. Malignancies are often reported within the first year of diagnosis. DM usually has a sub-acute onset and is progresses over months to years. Dysphagia has been reported to develop in 10 to 73% of patients with inflammatory myopathy during the clinical course and primarily affects the skeletal muscle-activated oropharyngeal phase of swallowing. The rapid onset and progression of disease despite use of high dose corticosteroids should ensue prompt evaluation for underlying malignancy. Conclusion As there is an increased risk of malignancy associated with DM, it is very important to have these patients undergo age appropriate cancer screening. Any new systemic symptoms or worsening disease despite appropriate immunosuppressive therapy should be given high index of suspicion with prompt evaluation for early diagnosis of malignancy. It is very critical to differentiate the dysphagia secondary to malignancy from that of DM for early diagnosis of an internal malignancy as described in our patient. Last Name: Abugroun First Author: Resident First Name: Ashraf Category: Clinical Vignette ACP Member: 3305083 Additional Authors: Colinagarcia Ibett, Fatima Ahmed, Potts Steven, Flicker Michael Title: The first report of Atovaquone/Proguanil-induced vanishing bile duct syndrome requiring liver transplant Abstract: CASE: A 62-year-old Caucasian male presented to the hospital with painless jaundice, pruritus, lethargy, dark urine and pale stool two weeks after having taken atovaquone/proguanil
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