This document contains a student portfolio from their clinical clerkship at Northside Medical Center. It includes a patient log with 18 patient encounters listing the chief complaint, subjective and objective findings, assessment, plan, and final diagnosis. It also includes 3 case discussions on atherosclerosis, Clostridium difficile colitis, and a lateral ankle sprain. Each case discussion covers the pathophysiology, differential diagnosis, findings to support the final diagnosis, and treatment options.

1. AMERICAN UNIVERSITY OF ANTIGUA
College of Medicine
Student Portfolio
Student Name:
Student ID Number:
Name of Hospital:
Type of Clerkship:
(Choose from Internal Medicine, Surgery, Pediatrics, Obstetrics & Gynecology, Psychiatry, Family Practice or enter an Elective)
Name of Specialty:
Start Date (mm/dd/yyyy): End Date (mm/dd/yyyy):
PART 1
Patient Log:
See Attached Spreadsheet
GAGANDEEP SINGH ANAND
NORTHSIDE MEDICAL CENTER
5TH SEMESTER
INTERNAL MEDICINE (3) + FAMILY PRACTICE (2)
09/23/2013 11/01/2013

2. Date Patient ISex IAge
Initials
PATIENT LOG
Subjective I Objective I Assessment
C.ut. •" 1,l...
Plan Final Diagnosis
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3. Case 1: (500 word maximum)
Case 2: (500 word maximum)
PART 2
List 3 cases and discuss in depth:
 Pathophysiology
 Differential Diagnosis
 Findings to Support Final Diagnosis
 Treatment Options
Mr. S is a 64 year-old male who presents with an improvement in shortness of breath since the day before. His condition improves when he sits up in
his bed than lying down flat. He reports generalized fatigue relieved upon resting. He recently got a CABG, before which he had surgery for a toe
amputation. He has had some trouble with moving bowels for 2 days and feels bloated.
Though this patient experiences shortness of breath, this patient has had a previous coronary artery bypass graft intervention. In this case the
pathophysiology is pertaining to atherosclerosis of coronary arteries. Atherosclerosis do not occur in a random fashion, hemodynamic factors interact
with activated vascular endothelium. Atherosclerotic plaques, may require 10 – 15 years for its full development. The major branches of the thoracic
and abdominal vessels as well as the large conduit vessels of the lower extremities are in high risk. One study suggests that low shear segments in
the coronary arteries develop greater necrotic core progression and constrictive remodeling whereas high shear segments develop greater necrotic
core and calcium progression, regression of fibrous and fibrofatty tissue, and excessive extensive remodeling. The first phase of atherosclerosis
histologically presents as focal thickening of the intima with an increase in smooth muscle cells and extracellular matrix. Lipids accumulate early in
fatty streak formation, this yields both intracellular and extracellular deposits. A small dermatan sulfate proteoglycan called by Biglycan, is detected in
the artherosclerotic coronary artery segments. This binds and traps lipoproteins, including apolipoprotein E, VLDL remnants, LDL, and HDL. The
fatty streak also consists of macrophages with a variable number of T lymphocytes. Macrophages are engorged with lipids are called foam cells, the
hallmark of the early atheroma. As these lesions expand, more smooth muscle cells migrate into the intima. The smooth muscle cells within the deep
layer of the fatty streak are susceptible to apoptosis, which is associated with further macrophage accumulation and micro vesicles that can calcify,
perhaps contributing to the transition of fatty streaks into atherosclerotic plaques.
Some of the differential diagnosis includes: angina pectoris, Buerger disease, dilated cardiomyopathy, coronary artery vasospasm, diabetes mellitus
[type1, type 2], giant cell arthritis, familial hypercholesterolemia, hypertension, myocardial ischemia, myocarditis, and many more.
A proper work up of atherosclerosis requires lipid studies, echo, nuclear imaging studies, CT, serum markers, C– reactive protein,coronary
angiography, ultrasonography.
Proper treatment requires a multitude of pharmacological strategies. It requires the treatment of low HDL levels and high triglyceride levels in
patients with diabetes, the use of ace inhibitors to reduce blood pressure, antiplatelet agents for acute coronary events, pharmacological treatment of
angina, revascularization procedures, and hormone therapy concerns.
http://emedicine.medscape.com/article/153647-differential
Ms. J is a pleasant 77 year-old female who presents with persistent diarrhea for 3 weeks, at 4-5 times/day. It is of watery consistency, brown color, foul
smell, with traces of blood – though the patient reports of internal hemorrhoids as a possible reason – no mucus, and of undigested food. The patient
reports increased urge to void after consuming a meal and a coinciding BM with micturation, in addition, she reports of a progressively worse frequency.
She does not report of any active pain, but of slight lower abdominal discomfort for 15-20mins after a BM. Ms. J reports of having a previous episode with
similar symptoms which was diagnosed as pseudo membranous colitis; she reports of no nausea, vomiting, sick contact or recent travel. Ms J also
reports of acute stress due to a sickness in the family, this could also present with GI symptoms. She was prescribed Flagyl (10 days), for which she is on
her 10th day. She was advised by her PCP to consume bananas and cheese to help with the diarrhea with no improvement. Ms. J reports having a dental
procedure one month ago in which amoxicillin (4 tabs) were used. She also stopped taking her monthly Simponi injections for her RA because she
believed it was the cause.
The pathophysiology of the C. Difficile is particularly specific to toxin A and B. once the normal colonic flora is disturbed, Clostridium difficile is able to
release toxins that cause you close of inflammation and damage.The toxins produced by Clostridium difficile are toxin a and toxin B, both are high
molecular weight proteins capable of binding to specific receptors on the intestinal mucosal hello there cells. These toxins gain entry within the cell by
catalyzing an alteration of the Rho proteins. These proteins help with actin polymerization, cytoskeleton architecture, and cell movement. Once this
protein is glycosylated the pathogenesis of Clostridium difficile appears.
Some differentials are Chron disease, diverticulitis, viral gastroenteritis, intra-abdominal sepsis, irritable bowel syndrome, malabsorption, salmonellosis,
shigellosis, ulcerative colitis, and vibrio.
Findings support clustered index of infection are leukocytosis, acute kidney injury, electrolyte imbalances, dehydration, hypoalbuminemia, and ansarca.
Guidelines indicate GDH EIA, and stool cytotoxin test. In addition, endoscope he can also be performed,wherein yellowish white 2 to10 mm plaques
overlying erythematous, edematous mucosa. In addition CT scanning can also be performed, where marked colonic wall thickening is the most common
or finding. Other features include ascites, irregularity of the bowel wall, and pericolonic stranding.
Treatment options include pharmacological management, fecalmicrobiota transplantation, and surgical intervention. Pharmacologically speaking in mild to
moderate infection patients should receive oral metronidazole or oral vancomycin, 10 – 14 days. In severe or severe – complicated infection, oral
vancomycin should be used for 10 – 14 days. In relapsed management the first recurrence requires metronidazole while the second recurrence requires
vancomycin. Though probiotics are not recommended treatment for active Clostridium difficile, it can be a supplement during preventative care.
http://emedicine.medscape.com/article/186458-overview

4. Case 3: (500 word maximum)
Ms. J is a pleasant 42 year-old female who presents with an acute left ankle sprain and reported through the ER this morning. She describes
spraining her ankle while walking down the stairs and laterally rolling the ankle. She reports a gradually improving, “on-and-off” pain with
inflammation, which is aggravated by lateral stretching and relieved by compression and elevation. She reports of using Ultram (synthetically
acting opiod analgesic) but has SE of itching. She also taking Celecoxib for her previous diagnosis of tenosynovitis. The patient also reports of
bed bug bites on her left arm and right thigh.
The lateral ankle complex is composed mainly of the anterior talofibular, calcaneofibular, and posterior talofibular ligaments, which is the most
commonly injured site. About 85% of such sprains aren inversion sprains of the lateral ligaments, while 5% are eversion sprains of the deltoid or
medial ligament. In addition 10% are syndesmotic sprains. An ATFL is the most likely component of the lateral angle complex to be injured in a
lateral ankle sprain. As well as during force dorsiflexion the PTFL can rupture. In the case of extreme external rotation this disrupts the deep
deltoid on the medial side and adduction in neutral and dorsiflexed position can disrupt the CFL. In the case of plantarflexion, the ATFL can be
injured. Ankle spurs may occur at any of the bony ligament attachments. It is quite common to see an anterior spur at the neck of the Tallus,
where the anterior ankle capsule attaches. This is a result of ossification of a hematoma organization associated with anterior ligament sprains.
Some differential diagnoses included a fracture where an individual with an ankle sprain can almost always walk on the foot albeit carefully and
with pain. Another diagnosis is neurovascular compromise, here we look for patient complaining of a cold foot and paresthesia. If pain persists
after rehabilitation, consider intra-articular meniscoid lesions, peroneal tendon subluxation, talar dome fracture, anterior process fracture,
complex regional pain syndrome. In addition Achilles tendon ruptures can also mimic ankle sprains. Other factors could be ankle impingement
syndrome, ankle fractures, gout ,navicular fracture, as well as stress fractures.
To do a work up consider plain radiographic imaging, stress view radiographic imaging, CT scanning, MRI, bone scanning,arthrographic
imaging.
Pain reduction is essential, but improvement of any loss of motion, strength, and or proprioception is equally important. A meta-analysis found
that neuromuscular rehabilitation results in more rapid improvements and function. For re-current lateral ankle sprains, treatment should begin
with trial of conservative therapy for approximately 2 to 3 months.
http://emedicine.medscape.com/article/1907229

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ACADEMIC ACTIVITIES (lECTURES/GRAND ROUNDS/CONFERENCES ETC.)
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7. Week
Faculty
Initial
PART3
Procedure Log:
See attached Spreadsheet
PART4
Academic Activities:
See attached Spreadsheet
Formal Case Presentations (If Applicable):
~e attached Spreadsheet
L,~c~ur~s/Gr;m{,i Rounds/ Conferel'lce Atte!lded:
See attached Spreadsheer
Faculty Comments
---__....
Weekly Faculty Sign-off
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