normalize. Magnetic resonance angiography of the abdomen revealed severe stenosis of the distal left renal artery consistent with FMD. The patient underwent contrast-enhanced renal artery angiography that confirmed the diagnosis. Balloon angioplasty of the stenotic left renal artery was performed. The day after angioplasty, the patient's plasma renin decreased to 50 microU/ml and BP to 130/70. IMPLICATIONS/DISCUSSION: Renovascular hypertension should be suspected in patients with age of onset before 20 or after 50 years, severe or refractory hypertension, acute rise in BP over previously controlled hypertension, rise in plasma creatinine concentration especially after starting an angiotensin-converting enzyme (ACE) inhibitor, abdominal bruit, absence of family history of hypertension, a unilateral small kidney, and recurrent acute pulmonary edema or unexplained heart failure. RAS may result from FMD or atherosclerotic disease. FMD most commonly affects women between the ages of 15 and 50 and accounts for less than 10% of cases of RAS. Atherosclerosis is responsible for the other 90% of cases. Gadolinium-enhanced magnetic resonance angiography is the best noninvasive imaging modality to diagnose RAS with 100% sensitivity and 95% specificity. Renal angiography is the gold standard to confirm the diagnosis. Percutaneous angioplasty is the treatment of choice for renovascular hypertension secondary to FMD. Patients with hypertension secondary to atherosclerotic RAS should be treated with aspirin, cholesterol-lowering agents, and smoking cessation. ACE inhibitors and diuretics can be used to control hypertension but should be avoided in the presence of bilateral stenosis. Balloon angioplasty is less successful in atherosclerotic RAS but placement of stents improves the success rates. Surgical revascularization should be considered in patients who fail angioplasty. LEARNING OBJECTIVES: 1. Identify a likely cause of recurrent painful blistering diseases in young adults 2. Identify the classical presentation, manifestations and prognosis of Epidermolysis Bullosa 3. Recognize the main management issues in caring for Epidermolysis Bullosa patients CASE INFORMATION: A 19 y/o latina woman presented for evaluation of painful blisters over her left hand and both feet after recent initiation of jogging. She reported a history of recurrent painful blisters affecting both her hands and feet since childhood. More severe blistering occured in areas where her skin was rubbed. Steroid creams provided no improvement. Lesions in the past healed over about a month, leaving hyper-pigmented scars. This current flare involved both her feet and left hand, but no other area. Systems review was negative. Other family members were not affected. She took Tylenol with hydrocodone for pain. On examination the patient had multiple blisters, 2±3 cm in diameter, mostly on the plantar surface of both feet. The soles of her feet were thickened and pigmented in circular patch-like forms. The blisters were exquisitely tender to touch. Initial differential diagnosis of this patient's condition included bullous pemphigoid, dermatitis herpetiformis, porphyria cutanea tarda and bullous SLE. A skin biopsy performed by a dermatologist demonstrated histologic separation of the basal layer. After immunohistochemistry, a diagnosis of epidermolysis bullosa, simplex form, was made. IMPLICATIONS/DISCUSSION: Epidermolysis Bullosa (EB) is the term given to three major groups of approximately 16 variants of rare dominant and recessive genetic diseases in which minor trauma causes non-inflammatory blistering (mechanobullous disease). There are as many as 150,000 Americans afflicted, mostly children, but variants present up to third decade of life. Those with medium to more severe kinds of EB can live into their thirties. Mortality is predominantly related to suprainfections. Management consists of all efforts to avoid trauma, particularly to the hands and feet via mittens and soft slippers. Adequate long-term pain control is a crucial aspect of taking care of EB patients, as is prevention and early treatment of supra-infections of the blistering lesions. Clasically all EB variants are resistant to all therapy, though literature reports exist of rare responders to treatment with Phenytoin, a known collagenase inhibitor, as well as IVIg. Genetic counseling is essential and fetal skin biopsy techniques have been developed for prenatal diagnosis. The diagnosis of glucagonoma was confirmed by pathologic examination. Upon removal of the tumor, her rash subsequently cleared without any complications. IMPLICATIONS/DISCUSSION: Glucagonoma syndrome is a rare syndrome with an estimated incidence of about 1 in 20 million people. It occurs with equal frequency in men and women and is usually detected between 40 to 60 years of age. The syndrome is caused by excessive production of glucagon by the alpha-secreting cells of the pancreas. Patients may have a characteristic rash, called``necrolytic migratory erythema'', that involves the perioral and perigenital regions. There may also be accompanying glossitis, angular chelitis, and blepharitis. The rash usually responds poorly to topical treatment. The only curative treatment for the syndrome is surgery. Glucagonoma syndrome should be considered in any patient with: 1) newly diagnosed diabetes and 2) a rash that does not resolve with proper topical treatment and is consistent with necrolytic migratory erythema. 10% of all strokes. There is a much broader differencial of disorders that cause infarction in younger people. Full evaluation is required to determine an underlying cause to treat patients accordingly and prevent recurrence. As opposed to stroke in the elderly which are often due to atherosclerosis and embolism, only 40% of strokes in the young are accounted for by these two etiologies. Other important causes include dissection, vasculitis, blood disorders, pregnancy, mitral valve prolapse, migraine, and patent foramen ovale. Given this patient had simulanteous anterior and posterior strokes, some of these etiologies are more likely, including: proximal emboli or a disseminated process such as vasculitis, blood disorder or drug use. This young person's stroke was a result of cocaine use. Proposed mechanisms by which cocaine causes stroke is that it induces vasoconstriction, vasospasm, hypertension and/or vasculitis. Case reports have documented stroke secondary to cocaine use in patients who had infarction in multiple distributions. Several of these cases were confirmed to have cocaine-induced vasculitis on autopsy despite having had negative MRA. LEARNING OBJECTIVES: To distinguish the toxicity of``crystal meth'' (methamphetamine) from other syndromes in a patient presenting with psychomotor agitation and tachycardia. CASE INFORMATION: A 22 year-old male with unremarkable PMH presented to the ED via ambulance with the acute onset of diaphoresis, tachycardia, and restlessness. He had been in police custody for approximately 48 hours, and charged with public intoxication. After his symptoms developed, he admitted to ingesting a``2 gram rock of crystal meth'' to avoid charges of illegal drug possession. Physical exam revealed an anxious but alert WM, BP 119/72 mm Hg, HR regular at 179 bpm, unlabored RR 16 per min., rectal temp T 99.3 degrees F, and O2 sat. 97% on RA. Auscultation of his chest was clear and his neurologic exam was nonfocal; but he was tremulous, pale, and his skin cold and clammy. He required substantial benzodiazepine doses to achieve sedation: diazepam 5mg IV en route to the ED, and a total of 8mg IV lorazepam and 14mg IV midazolam in the ED. The patient was electively intubated for``airway protection.'' His hospital course was uneventful; he was extubated within the first day of admission and transferred back to incarceration in 2 days. CPK levels were normal in the ED, but subsequently increased to ten times the ULN. A serum toxicology screen was positive for amphetamines and cannabinoids, and negative for salicylates, acetaminophen, methanol, ethanol, and ethylene glycol. Confirmatory testing revealed a serum methamphetamine level of 80,000 ng/dL. IMPLICATIONS/DISCUSSION: Delayed methamphetamine toxicity, defined as symptom onset 48 hours after ingestion, has not been previously reported in the medical literature. The crystalline form of methamphetamine, also known colloquially as``crank,'' is a stimulant drug of abuse that is usually nasally inhaled, snorted, or smoked. It is rapidly absorbed from any mucous membrane and produces almost immediate metabolic and psychotropic effects. This patient reported orally ingesting the drug in a plastic container, thus with gastrointestinal transit time and even partial digestion of the container, the drug may have been easily absorbed later in the distal GI tract. Alcohol withdrawal with incipient delirium tremens may also explain his presenting symptoms, but his markedly elevated CPK, a usual laboratory finding with acute methamphetamine overdose, and strongly positive serum methamphetamine level at the time of maximal symptomology, suggest methamphetamine toxicity as the etiology of his distress. This case stresses the need for medical personnel to obtain complete drug exposure histories from agitated patients, including explicit questioning with regard to drug ingestion stemming from attempts to conceal illegal activities.