MORNING REPORT FORMAT 5 points to the House with the last (reasonable) differential 5 points for the best summary 5 points to the House who correctly diagnoses the disease before the true diagnosis slide “Targaryen commits to pancreatitis due to hypertriglyceridemia.”

02 JULY 2018 VA MORNING REPORT SHAMYAL KHAN, DO

HPI CC: 72 YO M with two episodes of large bright red bloody bowel movements in the span of 1d HPI: Korean War Veteran presents with the above chief complaint. Similar event occurred three months ago but resolved. He has had fatigue with no weight loss. He denies abdominal pain or vomiting. Has had shortness of breath without cough but needs to ‘rest more often.’ He quit smoking 25 years ago and his most recent colonoscopy at 66 was negative.

ROS Bright red blood in stool x 2 Shortness of breath on exertion Intermittent dizziness Fatigue No cough, no wheezing No emesis No abdominal pain No chest pain No camping No recent travel history No change in diet

ADDL HISTORY PMHX: Hypertension, onychomycosis, tobacco abuse PSHX: Cholecystectomy 1999 Medications: 81 mg of ASA QD, Coreg 3.125 mg BID Allergies: Shellfish and red dye Family history: Adopted Social history: 8 years in the Navy, 20 pack year smoking history, rare EtOH consumption, no illicit drug use

DIFFERENTIAL DIAGNOSIS VASCULAR INFECTIOUS NEOPLASTIC DRUGS INFLAMMATORY/IDIOPATHIC CONGENITAL AUTOIMMUNE TRAUMA/TOXINS ENDOCRINE/ENVIORNMENT SOMETHING ELSE/PSYCH Diverticulosis (30%) Colitis (24%) Ischemic (12%) IBD (9%) Radiation (3%) Hemorrhoids (14%) Postpolypectomy (8%) Cancer/colon polyps (6%) Rectal ulcer (6%) AVMs (3%) Other (6%)

OBJECTIVE FINDINGS VITALS: BP 130/80 mmg Hg, P 88/min, RR 14/min, afebrile, sat 96% on RA GENERAL: Cooperative, well kept, elderly, in NAD HEENT: EOMI, PERRL, MMM, no JVD CV: Regular rate and rhythm, 3/6 mid-systolic ejection murmur LUNGS: CTAB, no accessory muscle use ABDOMEN: NT, NG, NR, no ascites SKIN: Senile purpura, dry EXT: +2 pulses bilaterally, no edema NEURO: CN intact, strength intact in all muscle groups, no sensory loss to temperature, light touch or pinprick GU: Bright red blood per rectum, no hemorrhoids

DIAGNOSTIC FINDINGS CMP – NL (Cr 1.0; BUN 16) CBC – Hgb 9.9, MCV 71, Plt 220, WBC 5.5 COAGs – INR 1.2, PTT 22 seconds CXR – No acute findings demonstrated EKG – Normal EGD – GI did this and said ‘I told you it would be negative.’ Colonoscopy – No acute findings of hemorrhoids, polyps, or ulcers. A few diverticula without active bleeding. Transthoracic echocardiogram – EF 60%, severe aortic stenosis

HOLD UP Next steps? Most likely diagnosis?

AND THE WINNER IS… PATHOPHYSIOLOGY: PRESENTATION: ANGIODYSPLASIA DUE TO ACQUIRED VWF DEFICIENCY PATHOPHYSIOLOGY: vWF is made and stored in megakaryocytes and endothelial cells. vWF forms adhesive bridges between platelets and endothelial surfaces Largest multimers thought to be the most active Protective carrier protein for Factor VIII. Acquired forms are immune and non-immune mediated (shear stress) vWF is thought to suppress angiogenesis PRESENTATION: Easy mild to moderate bleeding from mucosa, small skin cuts, heavy menstrual bleeding, post-partum bleeding

AND THE WINNER IS… DIAGNOSIS: TREATMENT: ANGIODYSPLASIA DUE TO ACQUIRED VWF DEFICIENCY DIAGNOSIS: CBC and PTT (although a normal PTT does not exclude) vWF antigen (VWF:Ag) – below 30 IU/dL is abnormal Ristocetin cofactor activity (VWF:Rco) Factor VIII:C TREATMENT: Treat underlying condition if necessary (AV replacement) Inherited forms do not respond to immunosuppressive therapies AVMs – Prophyalxis with VWF concentrates (two to three times a week) Factors that influence vWF levels -Physiologic stress -Type O has 25% less -Estrogens -Reduced in the African American population without reduced function

SOURCES UpToDate: Acquired von Willebrand syndrome MKSAP 17: Gastroenterology p 80 - 84