Today Dr. Heather Wickless from the Department of Dermatology at UT Southwestern gave a great, interactive lecture on skin conditions that internists should know about and how to evaluate and treat them. Below are takeaway points from her lecture:
Tinea versicolor is characterized by well-demarcated, tan, salmon, or hypopigmented patches, occurring most commonly on the trunk. KOH confirms the diagnosis.
Tinea pedis can be interdigital, moccasin, and vesiculobullous.
Candida intertrigo classically has satellite macules and papules or pustules around patches of erythema
If it scales, scrape it! KOH examination is the easiest and most cost effective method used to evaluate for fungal and yeast infections of the skin; culture can also aid in diagnosis.
Topical treatment is usually appropriate as a first-line agent for tinea pedis, tinea corporis, tinea versicolor, seborrheic dermatitis and candidal intertrigo, however oral medications are called for when involvement is extensive
Perioral dermatitis is an analogue of rosacea, and topical steroids may perpetuate the eruption.
When first line treatments fail, consider alternate diagnoses
“Shared decision making” is a term we often hear and referred to in health care as patients have become more educated about their health and want to be informed when making medical decisions. With recent spotlight in the media and medical literature on utility of tests and treatments, patients have even more questions for their providers. There is a resource for patients who want to know more about tests and treatments from the Informed Medical Decisions Foundation. This website provides links and articles that help guide a patient through clinic visits and what questions they may want to ask their provider. Also, there are links to online tools such as the cardiovascular disease risk calculator that patients can use. Thanks to Dr. Ethan Halm from the division of General Internal Medicine at UT Southwestern for the reference!
STRAIGHT FROM THE HOUSESTAFF – the April 2015 UT Southwestern Internal Medicine Journal Watch! They have summarized important issues in clinical practice, from alcoholic hepatitis to which medications to use for stroke prevention in afib. Make sure to take the EKG challenge at the end! You will have to view this post on our website to access the PDF. There is a quick run down of the topics below:
Corticosteroids in severe alcoholic hepatitis after recent upper GI bleed. Dr. Jan Petrasek reviewing Rudler et al., J Hepatol. 2015 Apr;62(4):816-21. 10.1016/j.jhep.2014.11.003. Epub 2014 Nov 11.
Serum ammonia level for the evaluation of hepatic encephalopathy. Dr. Jan Petrasek reviewing Ge et al., JAMA. 2014 Aug 13;312(6):643-4.
Extended report: Prediction of cardiovascular risk in rheumatoid arthritis: performance of original and adapted SCORE algorithms. Dr. Brian Skaug reviewing Arts, et al. Ann Rheum Dis. 2015 Feb 17. pii: annrheumdis-2014-206879. doi: 10.1136/annrheumdis-2014-206879
Trial of Early, Goal-Directed Resuscitation for Septic Shock [The Protocolised Management in Sepsis (ProMISe) Trial]. Dr. James Galloway reviewing Mouncey PR et al. N Engl J Med. 2015;372(14):1301-11.
A Randomized Trial of Icatibant in ACE-Inhibitor-Induced Angioedema. Dr. James Galloway reviewing Bas M, et al. N Engl J Med. 2015;372(5):418-25.
High-Sensitivity Troponin T and N-Terminal Pro-B-Type Natriuretic Peptide (NT-proBNP) and Risk of Incident Heart Failure in Patients with CKD: The Chronic Renal Insufficiency Cohort (CRIC) Study. Dr. Natalia Rocha reviewing Bansal N, et al. JASN 2015; 26:946-956
Preoperative renin–angiotensin system inhibitors use linked to reduced acute kidney injury: a systematic review and meta-analysis. Dr. Natalia Rocha reviewing Cheungpasitporn W, et al. Nephrol. Dial. Transplant. 2015; doi: 10.1093/ndt/gfv023
Which drug should we use for stroke prevention in atrial fibrillation? Dr. Douglas Darden reviewing Lau, Yee C.; Lip, Gregory Y.H. Current Opinion in Cardiology. 2014 July 29 (4): 293-300.
EKG CHALLENGE: Contributed by Dr. Jeanney Lew
All of the work above comes from the IMJW Editorial Board: Jan Petrasek, Brian Skaug, Ben Galloway, Natalia Rocha, Doug Darden, and Jeanney Lew!
A 46 year old female presents to clinic for followup of chronic cough (10 years duration). She was first evaluated 4 years ago with dry cough, diarrhea, and weight loss. She denies dyspnea, wheezing, sputum, or fevers. No travel or smoking history. No birds or occupational exposures. Seen by ENT, allergy, GI, speech therapy; she has had 24h ambulatory ph monitoring (no reflux found); laryngoscopy (no vocal cord dysfunction), skin testing for allergens (negative). She has been treated with BID Nexium, nasal steroids, inhaled steroids, systemic steroids, bronchodilators, leukotriene antagonists, and ipratropium with no change in cough. No rashes, joint pain, dysphagia, skin change, hair changes, fevers, chills, malaise or other symptoms.
T 98.5 HR 85 BP 111/72 RR 14 100% room air BMI 23
Gen: well appearing, mild coughing, no distress. Otherwise, exam is normal.
Pertinent negatives: no oral ulcers, no cardiac murmurs or rubs, clear lungs, no wheezes, normal effort, symmetric diaphragmatic excursion, no HSM, no skin rashes, no joint swelling or effusion, no nailbed changes, no sinus tenderness, normal tympanic membranes, no lymphadenopathy.
Today Dr. Bethany Agusala from the division of General Internal Medicine at UT Southwestern gave a lecture today on women’s health, focusing on cervical and breast cancer screening and post-menopausal management. Check out her slides below!
Antineutrophil cytoplasmic autoantibodies (ANCAs) are associated with, and are the probable cause of, a distinct form of vasculitis that can affect any organ in the body. Although small vessels are the predominant target, ANCA-associated vasculitis (AAV) can affect many different types of vessels including arteries, arterioles, capillaries, venules and veins. Immunopathologically, AAV has an absence or paucity of immunoglobulin deposition in injured vessels (pauci-immune vasculitis), compared with the more extensive deposition of immunoglobulin in immune-complex-mediated small-vessel vasculitis.1 AAV can be limited to one organ at the time of presentation (for example, lung-limited disease or renal-limited disease) or involve multiple organs. Frequent target tissues are the upper and lower respiratory tract, kidneys, skin and peripheral nerves. Onset and exacerbations induce signs and symptoms of high levels of circulating inflammatory cytokines, such as fever, arthralgia and myalgia. In addition to these nonspecific systemic inflammatory manifestations, inflammation of vessel walls causes more specific signs and symptoms of vasculitis depending on which vessels and which organs are affected, for example purpura caused by dermal venulitis; pulmonary haemorrhage caused by alveolar capillaritis; glomerulonephritis caused by glomerular capillaritis; peripheral neuropathy caused by epineural arteritis; and ocular inflammation caused by vasculitis in small vessels in the eye and orbit. In addition to vasculitis, some variants of ANCA-associated disease have extravascular necrotizing granulomatous inflammation (granulomatosis)—seemingly not arising from vascular inflammation—that most often affects the upper and lower respiratory tracts but can affect any organ.
AAV can also be classified on the basis of autoantigen specificity. In patients with vasculitis, the two best-documented autoantigen targets of ANCA are myeloperoxidase (MPO) and proteinase 3 (PR3). Classification of AAV by antigen specificity clearly shows differences in clinical presentations and outcomes, organ system involvement, patterns of extravascular inflammation, and genetic associations including HLA associations.
An important role for ANCAs in the pathogenesis of vasculitis and glomerulonephritis is supported by clinical evidence and by in vitro and in vivo experimental data. The leading theory proposes that circulating neutrophils and monocytes that have been primed by inflammatory stimuli display ANCA antigens at or near the cell surface, and that interaction of these antigens with ANCAs results in neutrophil activation and initiation of vascular inflammation. An extension of this theory proposes that primed extravascular neutrophils interact with interstitial ANCAs, causing necrotizing inflammation and resultant reactive granulomatous inflammation.
Nature Reviews Rheumatology | 10, 463–473 | (2014) doi:10.1038/nrrheum.2014.103 | Published online 08 July 2014
One of our residents, Udayan Shah (PGY-01), published an article online in JAMA Internal Medicine this week, “When Documentation Supersedes Patient Communication – An Example From An Endoscopy Unit” along with Dr. Deepak Agrawal from the division of Digestive and Liver Disease at UT Southwestern. The article focuses on question surveys that providers ask to patients including physicians and nurses. The authors discuss the utility of these surveys to patient care and why these surveys have become common in health care settings. Are these surveys mandated by an authorizing body like CMS or the Joint Commission? Do these surveys lead to better patient care and outcomes? Check out the article below to read more about this!
AIDS defining illness and typically seen in HIV patients with CD4<100 cells/microL.
The fungus (Histoplasma capsulatum) is found in soil contaminated with bird or bat excreta and transmission occurs from inhalation of spores.
Thought to be endemic in Ohio, Mississippi, Caribbean, Mexico, Asia, and Central/South America.
Immunocompromised hosts can present with more severe symptoms: fevers, night sweats, nausea, vomiting, dyspnea.
50% of AIDS patients with disseminated histoplasmosis have pulmonary involvement.
Elevated LFT’s, LDH, and ferritin are commonly seen. Elevated creatinine is considered a poor prognostic factor.
Although the initial chest x-ray often looks normal, may see diffuse interstitialor reticulonodular infiltrates.
Most sensitive and specific test for suspected disseminated histoplasmosis in an HIV patient is histoplasmosis antigen detection.
Histoplasmosis antigen can be detected in fluids including urine, serum, cerebrospinal fluid.
Rapid initiation of treatment is important and includes induction and maintenance phases. Amphotericin B is typically used for induction for 1-2 weeks. Therapy is then switched to itraconazole for consolidation and long-term suppression.
2009 IDSA guidelines recommend primary prophylaxis with itraconazole for HIV patients with CD4<150.