1. 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.”

2. 02 JULY 2018 VA MORNING REPORT SHAMYAL KHAN, DO

3. 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.

4. 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

5. ADDL HISTORY PMHX: Hypertension, onychomycosis, tobacco abuse
PSHX: Cholecystectomy 1999
Medications: 81 mg of ASA QD, Coreg 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

6. 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%)

7. 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

8. 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

9. HOLD UP
Next steps?
Most likely diagnosis?

10. 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

11. 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

12. SOURCES UpToDate: Acquired von Willebrand syndrome
MKSAP 17: Gastroenterology p