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interstitial cystitis samer kareem 2,759 Views • 2 years ago

Interstitial cystitis is a clinical syndrome characterized by daytime and nighttime urinary frequency, urgency, and pelvic pain of unknown etiology. Interstitial cystitis has no clear etiology or pathophysiology, and diagnostic criteria for the syndrome remain undefined. Despite considerable research, universally effective treatments do not exist; therapy usually consists of various supportive, behavioral, and pharmacologic measures. Surgical intervention is rarely indicated. The International Continence Society has coined the term painful bladder syndrome (suprapubic pain with bladder filling associated with increased daytime and nighttime frequency, in the absence of proven urinary infection or other obvious pathology) and reserves the diagnosis of interstitial cystitis for patients with characteristic cystoscopic and histologic features of the condition.[1] An international consensus panel was able to generally agree on the following definition of interstitial cystitis/bladder pain syndrome (IC/BPS): unpleasant sensation (pain, pressure, discomfort) perceived to be related to the urinary bladder and associated with lower urinary tract symptoms of more than 6 weeks duration, in the absence of infection or other identifiable causes. American Urological Association (AUA) guidelines published in 2011 and amended in 2014 use an evidence-based approach to provide a clinical framework for the diagnosis and management of this condition.[2, 3, 4] In 1887, Skene initially described a condition characterized by inflammation that destroyed the urinary bladder "mucous membrane partly or wholly and extended to the muscular parietes." Guy Hunner popularized the disease with the description of characteristic bladder wall ulcers in association with a symptom complex of chronic bladder inflammation.[5] The first comprehensive epidemiologic description of interstitial cystitis is credited to Hand, who in 1949 described the widespread, small, submucosal bladder hemorrhages and the significant variation in bladder capacity characteristic of the condition. Despite years of intensive research, there are no specific clinical or urinary markers currently clinically available; no absolutely specific radiographic, laboratory, or serologic findings; and no biopsy patterns that are pathognomonic for interstitial cystitis. Some research suggests that the following may all play a role in the disease pathophysiology: (1) pelvic floor dyfunction, (2) dysregulated immune or inflammatory signals, (3) neural hypersensitivity, and (4) disruption of the proteoglycan/glycosaminoglycan (GAG) layer.[6] Interstitial cystitis, howerver, remains a diagnosis of exclusion (see Presentation, DDx, and Workup.) Intensive study has been done to attempt to identify biomarkers for IC/BPS. Some interesting studies have shown that bladder nitric oxide is an accurate marker for Hunner lesions, but these are not present in all patients, and the test requires specific equipment, which has limited widespread clinical use.[7] Differences in levels of cytokines and chemokines, specifically CXCL-10, have shown some ability to differentiate patients with and without Hunner lesions.[8] Other studies of ulcerative IC/BPS have shown that numerous other cytokines and chemokines are up-regulated as well, heralding a possible urinary test to identify patients.[9] An additional substance shown to be up-regulated in IC/BPS patients is antiproliferative factor (APF). This small 8–amino-acid peptide has been associated with suppression of cell growth, increases in transcellular permeability, and lowering of levels of proteins that form intercellular junctional complexes. It is synthesized and secreted from bladder epithelial cells from patients with IC/BPS and may play a key role in pathophysiology.[10] In vitro studies have shown that removal of APF from cell culture media restored cell proliferation and membrane integrity.[11] Studies have also suggested APF in the therapeutic effect of hydrodistension in patients with IC/BPS, although further confirmatory studies are necessary.[12] The most important element in treating patients with interstitial cystitis is education and emotional support. Periodic exacerbations are managed as they occur because no long-term therapy has been shown to prevent or delay recurrent episodes. Therefore, the purpose of treatment is to palliate and alleviate symptoms. Because no discrete pathognomonic pathologic criteria exist for assessing and monitoring disease severity, indications and goals for treatment are based on the degree of patient symptoms. Assessing patient response to treatment is also complicated because of the subjective nature of symptoms; the waxing and waning nature of symptoms without treatment; and the lack of objective serologic, physical, or histopathologic findings. Conservative measures and oral or intravesical treatments are considered first-line treatment. (See Treatment.)

Herpes Simplex samer kareem 2,355 Views • 2 years ago

Primary infection with herpes simplex viruses (HSVs) is clinically more severe than recurrent outbreaks. However, most primary HSV-1 and HSV-2 infections are subclinical and may never be clinically diagnosed. Orolabial herpes Herpes labialis (eg, cold sores, fever blisters) is most commonly associated with HSV-1 infection. Oral lesions caused by HSV-2 have been identified, usually secondary to orogenital contact. Primary HSV-1 infection often occurs in childhood and is usually asymptomatic. Primary infection Symptoms of primary herpes labialis may include a prodrome of fever, followed by a sore throat and mouth and submandibular or cervical lymphadenopathy. In children, gingivostomatitis and odynophagia are also observed. Painful vesicles develop on the lips, the gingiva, the palate, or the tongue and are often associated with erythema and edema. The lesions ulcerate and heal within 2-3 weeks. Recurrences The disease remains dormant for a variable amount of time. HSV-1 reactivation in the trigeminal sensory ganglia leads to recurrences in the face and the oral, labial, and ocular mucosae. Pain, burning, itching, or paresthesia usually precedes recurrent vesicular lesions that eventually ulcerate or form a crust. The lesions most commonly occur in the vermillion border, and symptoms of untreated recurrences last approximately 1 week. Recurrent erythema multiforme lesions have been associated with orolabial HSV-1 recurrences. A recent study reported that HSV-1 viral shedding had a median duration of 48-60 hours from the onset of herpes labialis symptoms. They did not detect any virus beyond 96 hours of symptom onset.[7] Genital herpes HSV-2 is identified as the most common cause of herpes genitalis. However, HSV-1 has been increasingly identified as the causative agent in as many as 30% of cases of primary genital herpes infections likely secondary to orogenital contact. Recurrent genital herpes infections are almost exclusively caused by HSV-2. Primary infection Primary herpes genitalis occurs within 2 days to 2 weeks after exposure to the virus and has the most severe clinical manifestations. Symptoms of the primary episode typically last 2-3 weeks. In men, painful, erythematous, vesicular lesions that ulcerate most commonly occur on the penis, but they can also occur on the anus and the perineum. In women, primary herpes genitalis presents as vesicular/ulcerated lesions on the cervix and as painful vesicles on the external genitalia bilaterally. They can also occur on the vagina, the perineum, the buttocks, and, at times, the legs in a sacral nerve distribution. Associated symptoms include fever, malaise, edema, inguinal lymphadenopathy, dysuria, and vaginal or penile discharge. Females may also have lumbosacral radiculopathy, and as many as 25% of women with primary HSV-2 infections may have associated aseptic meningitis. Recurrences After primary infection, the virus may be latent for months to years until a recurrence is triggered. Reactivation of HSV-2 in the lumbosacral ganglia leads to recurrences below the waist. Recurrent clinical outbreaks are milder and often preceded by a prodrome of pain, itching, tingling, burning, or paresthesia. Individuals who are exposed to HSV and have asymptomatic primary infections may experience an initial clinical episode of genital herpes months to years after becoming infected. Such an episode is not as severe as a true primary outbreak. More than one half of individuals who are HSV-2 seropositive do not experience clinically apparent outbreaks. However, these individuals still have episodes of viral shedding and can transmit the virus to their sexual partners. Other HSV infections Localized or disseminated eczema herpeticum is also known as Kaposi varicelliform eruption. Caused by HSV-1, eczema herpeticum is a variant of HSV infection that commonly develops in patients with atopic dermatitis, burns, or other inflammatory skin conditions. Children are most commonly affected. Herpes whitlow, vesicular outbreaks on the hands and the digits, was most commonly due to infection with HSV-1. It usually occurred in children who sucked their thumbs and, prior to the widespread use of gloves, in dental and medical health care workers. The occurrence of herpes whitlow due to HSV-2 is increasingly recognized, probably due to digital-genital contact. Herpes gladiatorum is caused by HSV-1 and is seen as papular or vesicular eruptions on the face, arms, or torsos of athletes in sports involving close physical contact (classically wrestling). Disseminated HSV infection can occur in females who are pregnant and in individuals who are immunocompromised. These patients may present with atypical signs and symptoms of HSV, and the condition may be difficult to diagnose. Herpetic sycosis, a follicular infection with HSV, may present as a vesiculopustular eruption on the beard area. This infection often results from autoinoculation after shaving through a recurrent herpetic outbreak. Classically caused by HSV-1, there have been rare reports of relapsing beard folliculitis caused by type 2 HSV.[8] Neonatal HSV HSV-2 infection in pregnancy can have devastating effects on the fetus. Neonatal HSV usually manifests within the first 2 weeks of life and clinically ranges from localized skin, mucosal, or eye infections to encephalitis, pneumonitis, disseminated infection, and demise. Most women who deliver infants with neonatal HSV had no prior history, signs, or symptoms of HSV infection. Risk of transmission is highest in pregnant women who are seronegative for both HSV-1 and HSV-2 and acquire a new HSV infection in the third trimester of pregnancy. Factors that increase the risk of transmission from mother to baby include the type of genital infection at the time of delivery (higher risk with active primary infection), active lesions, prolonged rupture of membranes, vaginal delivery, and an absence of transplacental antibodies. The mortality rate for neonates is extremely high (>80%) if untreated.

Pediatric Surgical Fellowship - Nemours/Alfred I. duPont Hospital for Children hooda 217 Views • 2 years ago

Train with some of the region’s very best pediatric general surgeons — in a two-year, pediatric surgical fellowship training program at Nemours/Alfred I. duPont Hospital for Children. Our hospital’s Division of Pediatric Surgery is offering this program in affiliation with Sidney Kimmel Medical College at Thomas Jefferson University .

The goal of the fellowship is to give individuals who have completed an accredited general surgery residency advanced knowledge and training in the management and surgical treatment of newborns, infants and children.

Our Fellowship Program
This fellowship will help you prepare for certification by the American Board of Surgery, and is accredited by the Accreditation Council for Graduate Medical Education (ACGME).

The Pediatric Surgery Fellowship aims to:

train a well-rounded, empathetic, safe pediatric surgeon who is confident managing all aspects of the surgical care of children.
steward our fellow in quality improvement projects and methodology, and provide research opportunities.
provide a rigorous didactic curriculum for our fellow utilizing 360 degree feedback.
cultivate opportunities for our fellow to educate residents and students.
encourage our fellow to collaborate across specialties.
develop our fellow’s presentation skills during M&M conferences and multi-disciplinary educational meetings.
The program features the full participation of all nine of the pediatric surgical division’s full-time faculty members. Each of these physicians will contribute greatly to your education. Your training will include operating room and outpatient clinic experience, as well as bedside evaluation of children. You’ll also play a role in the organization of formal teaching conferences, held weekly. Formal rotations will be spent on Pediatric Urology, PICU and Neonatology during the first 12 months. The last year will be spent entirely on the Pediatric Surgical Service.
The majority of your inpatient consultative time will take place at Nemours/Alfred I. duPont Hospital for Children, a freestanding children’s hospital in Wilmington, Del. The hospital:

is nationally ranked by U.S. News & World Report in eight pediatric specialties
recently opened expansion with 260 beds
performs more than 2,800 inpatient and 9,300 outpatient surgical procedures each year in our operating rooms
has an on-site delivery center for newborns with complex congenital anomalies
receives more than 50,000 annual visits in our Emergency Department (ED)
is accredited by The American College of Surgeons as a Level One Pediatric Trauma Center
is accredited by the Commission on Accreditation of Rehabilitation Facilities (CARF)

Visit https://www.nemours.org/educat....ion/gme/fellowships/ to learn more.

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