Evaluation of Syncope

Evaluation of Syncope

This illustration is one of the latest editorial pieces completed for the American Academy of Family Physicians featuring The Evaluation of Syncope.

Syncope is a brief and transient loss of consciousness with complete return to pre-existing neurologic function.  It is classified as neurally-mediated, orthostatic, cardiac and neurogenic.  The elderly are likely to have orthostatic, carotid sinus hypersensitivity or cardiac syncope, whereas, younger patients are more likely to have neurally-mediated syncope.  Common non-syncope syndromes with similar presentations include seizures, metabolic syndromes, acute intoxication,psychiatric disorders and cerebrovascular events.

The majority of patients presenting with unexplained syncope will require admission.  Several risk stratification tools have been investigated to assess the risk of short-term death and need for immediate hospitalization.  All patients presenting with syncope except vasovagal are at increased risk of death from any cause. The AHA/ACCF syncope guidelines present an algorithmic approach for the evaluation of syncope.

The most important diagnostic tool remains the history and physical examination.  All patients presenting with syncope require an electrocardiogram, orthostatic vital signs and interval monitoring.  Patients diagnosed with neurally-mediated or orthostatic syncope usually require no additional testing.  In cases of unexplained syncope, further testing such as electrocardiographic monitoring, echocardiogram, ischemic evaluation and electrophysiological studies may be required.  Although a small subset of patients will remain undiagnosed, those undergoing comprehensive evaluation are unlikely to have a recurrent syncope event.

View illustration

Failed Total Shoulder Arthroplasty

Failed Total Shoulder Arthroplasty

This illustration was commissioned for Arthroscopically Assisted Conversion of Total Shoulder Arthroplasty to Hemiarthroplasty With Glenoid Bone Grafting by Surena Namdari, MD, MSc; and David Glaser, MD for publication in ORTHOPEDICS October 2011 issue (ORTHOPEDICS November 2011;34(11):862).

Aseptic loosening of the glenoid component after total shoulder arthroplasty presents a considerable treatment challenge in the setting of substantial glenoid bone loss.  Glenoid component explantation and bone grafting of defects has become a common methods of recreating bone stock in hopes of preventing later fractures, maintaining joint kinematics, and allowing for later glenoid reimplantation if necessary.  While this has been traditionally accomplished via open techniques, we describe an arthroscopic-assisted method of glenoid explantation and bone grafting for cases of aseptic glenoid loosening with contained bone defects.

Natural Killer Cells

Natural Killer Cells

This illustration was created for a feature article in the October 2011 issue of the Washington University in St. Louis Alumni Magazine article by Steve Kohler.

“Professor Wayne Yokoyama, MD, long intrigued by the function of natural killer (NK) cells, has shown that NK cells, using a “licensing strategy,” are vitally important elements of the immune system. In 2010, on the occasion of accepting the Lee C. Howley Sr. Prize for his pioneering arthritis research, Wayne M. Yokoyama, MD, told his audience that real advances in science do not come from the close application of previously known arcane facts to solve difficult problems. Rather, he said, science requires taking risks to venture completely beyond what is known, pursuing nature’s secrets that she is not inclined to reveal easily. “There is art to science,” according to Yokoyama, who holds the Sam J. and Audrey Loew Levin Chair for Research in Arthritis.

A major leap in thinking then was required to realize that NK cells bind to MHC-1 just as T-cells do, but work in the opposite fashion. “When an NK cell sees an MHC-1 molecule, it doesn’t note that there is a foreign peptide being displayed. Instead, its job is to patrol for self, and when it binds to MHC-1, the NK cell is shut off,” Yokoyama explains. “Only when the self signal is insufficient is the NK cell released from its ‘off’ condition and freed to do its work.” That’s vitally important information, because viruses have evolved to depress MHC-1 in their attempt to evade T-cells. So NK cells serve an important role as a fail-safe in the immune system, effective when another of the body’s defenses has been blinded by tricky infections.

When an NK cell sees an MHC-1 molecule, it doesn’t note that there is a foreign peptide being displayed. Instead, its job is to patrol for self, and when it binds to MHC-1, the NK cell is shut off. Only when the self signal is insufficient is the NK cell released from its ‘off’ condition and freed to do its work,” Yokoyama explains. “That’s not the whole story, however, because NK cells also need to be activated.” (Illustration by Jennifer E. Fairman, CMI, FAMI)

Read the October 2011 Washington University in St. Louis Magazine article here: Rheumatologist Cracks Molecular Mystery.

Angiogenesis Targeting

Angiogenesis Targeting

TTV 02 Angiogenesis Targeting: Mechanism of action animation that explains angiogenesis and it’s roll in cancer growth. VEGF factors in anti-angiogenic activity, helping to stop and reverse cancer growth and proliferation. Angiogenesis can be targeted by various types of drug agents (EGFR or HER1, VEGF, VEGF receptor and MMP inhibitors) which can interrupt the growth of tumor vasculature. Storyboard, Illustration and Animation by Jennifer Fairman.

TTV 02: Angiogenesis Targeting from Fairman Studios on Vimeo.

Angiogenesis can be targeted by various types of drug agents (EGFR or HER1, VEGF, VEGF receptor and MMP inhibitors) which can interrupt the growth of tumor vasculature. Storyboard, Illustration and Animation by Jennifer Fairman.

Normal vs. Tumor Vasculature

Normal vs. Tumor Vasculature

TTV 01 Normal vs. Tumor Vasculature: Mechanism of action animation that explains angiogenesis and it’s roll in cancer growth. VEGF factors in anti-angiogenic activity, helping to stop and reverse cancer growth and proliferation. Understanding normal vs. tumor vasculature and the relationship of tumor induced blood vessels with angiogenic mechanisms of action. Storyboard, Illustration & Animation by Jennifer Fairman.

TTV 01: Normal vs. Tumor Vasculature from Fairman Studios on Vimeo.

Understanding normal vs. tumor vasculature and the relationship of tumor induced blood vessels with angiogenic mechanisms of action. Storyboard, Illustration & Animation by Jennifer Fairman.

The Role of EGFR

The Role of EGFR

MTT 02 The Role of EGFR in Angiogenesis: Mechanism of action animation that explains angiogenesis and it’s roll in cancer growth. VEGF factors in anti-angiogenic activity, helping to stop and reverse cancer growth and proliferation. Storyboard, Illustration & Animation by Jennifer Fairman. Mechanism of action animation that explains angiogenesis and it’s roll in cancer growth. VEGF factors in anti-angiogenic activity, helping to stop and reverse cancer growth and proliferation. HER1 & HER2 (EGFR) are shown to play a key role in cancer cell proliferation by their signalling cascade within cancer cells. Storyboard, illustration and animation by Jennifer Fairman.

MTT 02: The Role of EGFR from Fairman Studios on Vimeo.

Mechanism of Action animation. HER1 & HER2 (EGFR) are shown to play a key role in cancer cell proliferation by their signalling cascade within cancer cells. Storyboard, illustration and animation by Jennifer Fairman.

error: Content is on this site is monitored and © protected.