A Brief Dermatology Curriculum in Skin Cancer Detection and Prevention to Improve Medical Student Knowledge and Confidence.

Introduction: While the incidence of skin cancers continues to rise, there remains a disproportionate lack of introductory training on skin cancer screening and identification of modifiable behaviors in medical curricula. Trainees and students have cited low confidence in their ability to counsel patients and lack of instruction as barriers. Methods: To address this need, we created a 1-hour didactic lecture based on a cognitive teaching framework for third-year medical students during their core primary care clerkship. The session highlighted visual identification of different skin cancers, factors increasing individual risk, and photoprotective behaviors. Session content was based on American Academy of Dermatology recommendations for skin cancer prevention. An assessment of knowledge, behaviors, and attitudes given before, immediately following, and at 6 months after the session was used to determine efficacy. Results: One hundred eight students before and immediately after the session demonstrated significantly improved knowledge (mean correct: 71% presession vs. 99% postintervention, p < .0001). Based on 39 participants completing 6-month follow-up, knowledge remained improved (mean answered correctly: 80%, p < .0001). Confidence in patient counseling on preventive behaviors, risk assessment, and reported likelihood of counseling significantly increased across the three time points (p < .0001 for all attitude questions). Specific topics included appropriate referral to a dermatologist, sunscreen application, and dangers of indoor tanning bed usage. Discussion: Our session on skin cancer screening and prevention demonstrated improvements in medical student knowledge, confidence, and patient counseling likelihood. This introductory curriculum could be adapted for multiple core clerkships or specialties.

Superior vena cava obstruction associated with nephrogenic systemic fibrosis.

A 56-year-old woman with hypertension-induced end stage renal disease presented with skin thickening and mottled discoloration. Cutaneous biopsy showed increased dermal fibroblasts embedded in fibromyxoid stroma with scattered perivascular and interstitial mononuclear cells. Immunohistochemistry revealed prominent CD34+ dendritic cells in septal spaces, consistent with Nephrogenic Systemic Fibrosis (NSF). Seven years and two years prior she had received a gadolinium-based contrast agent (GBCA). She died due to NSF. Gross autopsy revealed a thickened and stenotic superior vena cava (SVC). Extensive fibrosis of the SVC, dermis, and subcutaneous tissue was noted, together with hyalinized collagen fibers within the muscular wall of the intestines and dura mater. These findings support the importance of skin changes in the recognition of life threatening extracutaneous tissue involvement in NSF.

Mechanism of loss of Kv11.1 K+ current in mutant T421M-Kv11.1-expressing rat ventricular myocytes: interaction of trafficking and gating.

BACKGROUND: Type 2 long QT syndrome involves mutations in the human ether a-go-go-related gene (hERG or KCNH2). T421M, an S1 domain mutation in the Kv11.1 channel protein, was identified in a resuscitated patient. We assessed its biophysical, protein trafficking, and pharmacological mechanisms in adult rat ventricular myocytes. METHODS AND RESULTS: Isolated adult rat ventricular myocytes were infected with wild-type (WT)-Kv11.1- and T421M-Kv11.1-expressing adenovirus and analyzed with the use of patch clamp, Western blot, and confocal imaging techniques. Expression of WT-Kv11.1 or T421M-Kv11.1 produced peak tail current (I(Kv11.1)) of 8.78±1.18 and 1.91±0.22 pA/pF, respectively. Loss of mutant I(Kv11.1) resulted from (1) a partially trafficking-deficient channel protein with reduced cell surface expression and (2) altered channel gating with a positive shift in the voltage dependence of activation and altered kinetics of activation and deactivation. Coexpression of WT+T421M-Kv11.1 resulted in heterotetrameric channels that remained partially trafficking deficient with only a minimal increase in peak I(Kv11.1) density, whereas the voltage dependence of channel gating became WT-like. In the adult rat ventricular myocyte model, both WT-Kv11.1 and T421M-Kv11.1 channels responded to ß-adrenergic stimulation by increasing I(Kv11.1). CONCLUSIONS: The T421M-Kv11.1 mutation caused a loss of I(Kv11.1) through interactions of abnormal protein trafficking and channel gating. Furthermore, for coexpressed WT+T421M-Kv11.1 channels, different dominant-negative interactions govern protein trafficking and ion channel gating, and these are likely to be reflected in the clinical phenotype. Our results also show that WT and mutant Kv11.1 channels responded to ß-adrenergic stimulation.