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Reidy and Bullous Bullous and Reidy blowin over bear bottles. :L in a tent on his back garden another random video from my phonee

Pemphigus Herpetiformis Dr. Wendy Levinbook, MD discusses Pemphigus Herpetiformis. See more at PLEASE RATE AND COMMENT!!! The mean age of onset of pemphigus herpetiformis (PH) is 65 years of age. Males and females are affected equally. Clinically, PH resembles dermatitis herpetiformis with red, vesicular, bullous, or papular lesions, often in a herpetiform pattern. Severe pruritus is characteristic. Oral mucous membranes may be involved. Light microscopic findings may be similar to pemphigus vulgaris with eosinophilic spongiosis and acantholysis. However, findings on histologic exam vary greatly and may not be helpful at the outset. Direct and indirect immunofluorescence demonstrate intercellular IgG primarily in the upper epidermis targeting desmoglein 1. Rarely, desmoglein 3 may be the target antigen. PH typically follows a benign course. Patients respond well to treatment with a tendency to develop complete remission. However, the disease course in some patients may evolve into a picture resembling pemphigus vulgaris or pemphigus foliaceus.

DALK and DMEK from one cornea One donor cornea for two corneal grafts of two patients ( one keratoconus, second - Pseudophakic Bullous Keratopaty) : Big Bubble Deep Anterior Lamellar Keratoplasty + Descemet Membrane Endothelial Keratoplasty

Regurgitate - Bullous Impetigo (clip) Regurgitate - Bullous Impetigo taken from the Effortless Regurgitation Of Bright Red Blood album that was released by Lowland Records in 1994

Viral Bullous Myringitis This video shows blebs or vesicles caused by viral inflammation in acute myringitis. It usually presents as earache accompanying or following upper respiratory tract infection or flu.

Dr Stephen Clarke pt 3 2010 JC Bystryn Pemphigus & Pemphigoid Meeting: From the Bench to the Bedside November 5-6, 2010 in Bethesda MD B Cells in Human SLE A copy of the slides can be found at

Dr Kim Yancey 2010 JC Bystryn Pemphigus & Pemphigoid Meeting: From the Bench to the Bedside November 5-6, 2010 in Bethesda MD Molecular mechanisms of dermal-epidermal separation in bullous pemphigoid vs. mucous membrane pemphigoid A copy of the slides can be found at

Dr Janet Fairley 2010 JC Bystryn Pemphigus & Pemphigoid Meeting: From the Bench to the Bedside November 5-6, 2010 in Bethesda MD Anti-IgE therapy of bullous pemphigoid A copy of the slides can be found at

Dr Stephen Clarke pt 1 2010 JC Bystryn Pemphigus & Pemphigoid Meeting: From the Bench to the Bedside November 5-6, 2010 in Bethesda MD B Cells in Human SLE A copy of the slides can be found at

Dr Stephen Clarke pt 2 2010 JC Bystryn Pemphigus & Pemphigoid Meeting: From the Bench to the Bedside November 5-6, 2010 in Bethesda MD B Cells in Human SLE A copy of the slides can be found at

Dr Carlo Pincelli 2010 JC Bystryn Pemphigus & Pemphigoid Meeting: From the Bench to the Bedside November 5-6, 2010 in Bethesda MD Review of Fas system involvement A copy of the slides can be found at

Dr John Stanley pt 2 2010 JC Bystryn Pemphigus & Pemphigoid Meeting: From the Bench to the Bedside November 5-6, 2010 in Bethesda MD Pathogenic scFv & V genes from pemphigus vulgaris autoantibodies A copy of the slides can be found at

Dr Grant Anhalt pt 1 2010 JC Bystryn Pemphigus & Pemphigoid Meeting: From the Bench to the Bedside November 5-6, 2010 in Bethesda MD Review of Rituxan A copy of the slides can be found at

Dr Luis Diaz pt 1 2010 JC Bystryn Pemphigus & Pemphigoid Meeting: From the Bench to the Bedside November 5-6, 2010 in Bethesda MD Diversity of the autoantibody response in pemphigus (IgM, IgE, IgG subclasses) A copy of the slides can be found at

New Safety Information on Tarceva New information has been added to the labeling of the chemotherapy drug Tarceva (erlotinib). The revised labeling now warns about three kinds of serious adverse events: •Gastrointestinal perforation, which may be fatal. This risk is increased in patients receiving concomitant anti-angiogenic agents, corticosteroids, NSAIDs, or taxane-based chemotherapy, and it is also greater in those with a history of peptic ulceration or diverticular disease. Tarceva should be permanently discontinued if the patient develops gastrointestinal perforation. • Bullous, blistering and exfoliative skin conditions, possibly including Stevens-Johnson syndrome and toxic epidermal necrolysis, which can be fatal. Tarceva treatment should be interrupted or discontinued if the patient develops one of these conditions. •Ocular disorders, including corneal perforation or ulceration. Tarceva should be interrupted or discontinued if the patient experiences symptoms of an acute or worsening eye disorder, such as eye pain. FDA Patient Safety News: July 2009 For more information, please see our website: www.accessdata.fda.gov

SCUBA technique for DMEK donor preparation Harvesting donor tissue for endothelial keratoplasty with the Submerged Cornea Using Backgrounds Away technique is easy, consistent, and inexpensive. The SCUBA technique was first presented at a course with Dr. Melles at the AAO in 2007. This video was presented at AAO in 2008. It shows some of the nuances that may be helpful to those interesting in starting pure EK surgery. Wishing you all the best! ; )

Rhegmatogenous bullous retinal detachment.wmv Scleral buckle, PPV, PFCL, endolaser, PFCL/Air exchange, silicone oil for treatment of Rhegmatogenous bullous retinal detachment in one-eye myopic lady. Khaled Abdelgalil Shalaby, MD Al-Azhar University Cairo- Egypt Chief Vitreoretinal Service Dr Soliman Fakeeh Hospital Jeddah- KSA

Dr John Zone 2010 JC Bystryn Pemphigus & Pemphigoid Meeting: From the Bench to the Bedside November 5-6, 2010 in Bethesda MD Role of IgE in the pathogenesis of bullous pemphigoid A copy of the slides can be found at

New Safety Information on Tarceva (July 2009) New information has been added to the labeling of the chemotherapy drug Tarceva (erlotinib). The revised labeling now warns about three kinds of serious adverse events: • Gastrointestinal perforation, which may be fatal. This risk is increased in patients receiving concomitant anti-angiogenic agents, corticosteroids, NSAIDs, or taxane-based chemotherapy, and it is also greater in those with a history of peptic ulceration or diverticular disease. Tarceva should be permanently discontinued if the patient develops gastrointestinal perforation. • Bullous, blistering and exfoliative skin conditions, possibly including Stevens-Johnson syndrome and toxic epidermal necrolysis, which can be fatal. Tarceva treatment should be interrupted or discontinued if the patient develops one of these conditions. • Ocular disorders, including corneal perforation or ulceration. Tarceva should be interrupted or discontinued if the patient experiences symptoms of an acute or worsening eye disorder, such as eye pain.

Femtosecond assisted intrastromal CXL for bullous keratopathy

Bullous Pemphigoid - USMLE Study Songs Visit to download this song and for a better way to navigate these videos. Because all music should be free, I'm giving mine away: USMLE Study Songs and USMLEntertainment are my Step 1 series. In this series, Substance P presents a brief video review of a pertinent medical topic and writes an accompanying song. The song appears as a "response" to this video (or vice versa). See my YouTube home page for my disclaimer, and please visit my website. If you are offended by this video, please read my YouTube profile before commenting. I am not making fun of your disease or anyone's disease! These songs are designed to consolidate scientific information and make that information more memorable. --------------------- In the style of the Beach Boys, Pet Sounds era... easily my favorite album of all time.

My mates gammy leg thing!!!! yuk!!! My m8 awoke one day to find this in his leg!!!!! wtf!!! lol apparently called bullous pemphigoid!! anyone else had this?

Bullous Pemphigoid and Pemphigus Vulgaris - USMLEntertainment A catch-up video for my USMLE Step 1 series... Each weekSubstance P presents a brief video review of a pertinent medical topic and writes an accompanying song. The song appears as a "response" to this video shortly after publication. See my YouTube home page for my disclaimer, and visit my blog (web address above) to read the script for this week's video.

Epidermolysis Bullosa Acquisita Dr. Wendy Levinbook, MD discusses Epidermolysis Bullosa Acquisita. See more at PLEASE RATE AND COMMENT!!! This is a mechanobullous subepidermal autoimmune blistering disorder that usually begins in adulthood. Patients with epidermolysis bullosa acquisita (EBA) should have a negative family and personal history of blistering disorders in order to make the diagnosis. The classic presentation consists of skin fragility, noninflammatory bullae, and erosions in an acral distribution that heal with scarring and milia formation. Nail dystrophy and scarring alopecia may also be present. About one quarter of EBA patients will have a more inflammatory presentation similar to bullous pemphigoid patients with widespread, tense bulllae on inflamed or urticarial skin of the trunk and extremites. Rarely, these patients will present with only urticarial plaques. Pruritus is a prominent feature. About 10% of patients will present with mostly mucosal involvement similar to that seen in patients with cicatricial pemphigoid. Finally, a small number of patients will have a clinical presentation reminiscent of Brunsting-Perry cicatricial pemphigoid with vesiculobullous lesions localized to the head and neck that heal with residual scars. Histopathologic exam reveals a subepidermal blister. Patients with the more classic presentation demonstrate a sparse inflammatory infiltrate while lesions reminiscent of bullous pemphigoid have a more significant inflammatory infiltrate with ...

Dr John Stanley pt 1 2010 JC Bystryn Pemphigus & Pemphigoid Meeting: From the Bench to the Bedside November 5-6, 2010 in Bethesda MD Pathogenic scFv & V genes from pemphigus vulgaris autoantibodies A copy of the slides can be found at

Regurgitate - Bullous Impetigo Song: Bullous Impetigo Band; Regurgitate Album: Effortless Regurgitation of Bright Red Blood Year: 1994 Track list: 1. "Intro: The Act of Intestinal Regurgitation" - 1:13 2. "Disgorging Foetus" - 1:21 3. "Confluent Macular Drug Eruption" - 0:23 4. "Bullous Impetigo" - 1:22 5. "Fleshfeast" - 1:05 6. "Anorectal Ulceration" - 0:55 7. "Vulva Fermentation" - 0:33 8. "Multicystic Kidney" - 1:33 9. "Mucupurulent Offal Grinder" - 0:18 10. "Total Dismemberment of a Female Corpse" - 1:07 11. "Carnal Cacophony" - 0:47 12. "Vomit Breath" - 0:20 13. "Complete Rectal Prolapse" - 1:00 14. "Testicular Trauma" - 1:11 15. "Genital Cancer" - 1:53 16. "Malignant Tumor" - 1:20 17. "Diffuse Systemic Scerosis" - 0:19 18. "Owner of a Necrotic Intestine" - 0:37 19. "Newborn Regurgitation" - 0:51 20. "Torsion of the Testicle" - 0:32 21. "Worm Eaten Rectum" - 0:50 22. "Chronic Lymphatic Leukemie" - 1:23 23. "Metal Ulcer" - 0:34 24. "Purulent Discharge from the Urethra" - 1:10 25. "Vaginal Obstriction" - 1:14 26. "Cloudy, Grayish Vomitus" - 0:22 27. "Fleshmangler" - 1:08 28. "Splattered Brains" (Agathocles coper) - 1:00 29. "Bulging Vaginal Septum" - 0:39 30. "Acute Urinary Infection" - 1:08 31. "Severe Necroses of the Face" - 0:22 32. "Bleeding Peptic Ulcer" - 0:43 33. "Face Mutilation" - 0:35 34. "Extensive Ulcerative Tumor" - 0:41 35. "Tumecent Foetal Fluids to Expurgate" - 0:55 36. "Carbonized Bowels - 0:43 37. "Effortless Regurgitation of Bright Red Blood" - 1:18 *All music written by ...

Bullous Pemphigoid Treatment Dr. Wendy Levinbook, MD discusses Bullous Pemphigoid Treatment. See more at PLEASE RATE AND COMMENT!!! For mild, localized disease, topical steroids may be effective. Oral antibiotics such as tetracycline, minocycline, or erythromycin with or without niacinamide may also provide good treatment results in select patients with localized or generalized BP. Sulfones, such as dapsone or sulfapyridine may also be tried. These have been reported to be effective in up to 44% of BP patients. However, the mainstay of therapy in patients who fail to respond to antibiotics or to dapsone is treatment with systemic corticosteroids. Adjuvant immunosuppressive therapy with azathioprine or cyclophosphamide may be necessary in patients with severe disease and may be steroid-sparing. Other therapies with reported benefit include plasmapheresis and itravenous gammaglobulin.

Diagnosis of Bullous Diseases Dr. Wendy Levinbook, MD discusses Diagnosis of Bullous Diseases. See more at PLEASE RATE AND COMMENT!!! The diagnosis of bullous disorders is made by thorough clinical evaluation and is confirmed by histopathologic and immunofluorescent examination. Light microscopy will provide information on whether or not there is an inflammatory infiltrate and on the nature of the inflammatory infiltrate. In addition, it is a useful tool to determine the level of blister formation, that is intraepidermal or subepidermal. Electron microscopic examination provides more detailed information on the blister cleavage plane, but it is not routinely used for diagnostic purposes. Immunofluorescence is a laboratory technique for demonstrating the presence of tissue-bound and circulating antibodies and complement. Tissue-bound antibodies are demonstrated by direct immunofluorescence and circulating antibodies are demonstrated by indirect immunofluorescence. These laboratory techniques, in conjunction with a detailed history and a careful physical examination will lead the clinician to the correct diagnosis in most circumstances.

Dr Annette Czernik 2010 JC Bystryn Pemphigus & Pemphigoid Meeting: From the Bench to the Bedside November 5-6, 2010 in Bethesda MD Review of IVIG in pemphigus and pemphigoid & mechanism of action A copy of the slides can be found at

New Historicism (Koala Yo' Mama) Made for Mr. Burdick's English 2 class, an unsuspecting student contracts bullous pemphigoid from a bully who takes offense to his shirt. Starring Peter Wilson and Mike Moody.

Bullous Pemphigoid Dr. Wendy Levinbook, MD discusses Bullous Pemphigoid. See more at PLEASE RATE AND COMMENT!!! This disorder typically affects patients over 60 years of age, but it can rarely occur in children. There is no racial or ethnic predilection and the incidence is equal in males and females. Clinically, bullous pemphigoid (BP) is characterized by large tense bullae that are often preceded by red, urticarial patches or plaques. Lesions are most commonly located on the lower abdomen, inner thighs, and flexor forearms although they may occur anywhere. Mucous membrane involvement is uncommon. Lesions are usually associated with marked pruritus but they do not scar. BP is an acquired autoimmune disorder that occurs secondary to the formation of antibodies that interact with bullous pemphigoid antigen 1 (230 kDa intrahemidesmosomal antigen) and bullous pemphigoid antigen 2 (180 kDa hemidesmosomal transmembrane antigen, also known as type XVII collagen). This interaction is then followed by an inflammatory response leading to dermal-epidermal separation. On electron microscopic exam, blister formation occurs in the lamina lucida, between the basal cell membrane and the lamina densa. On histopathologic exam, lesions show a subepidermal blister with fluid, fibrin, and inflammatory cells including numerous eosinophils. Direct IF of perilesional skin demonstrates linear C3 and IgG. Indirect IF using normal stratified squamous epithelia (such as human epidermis or monkey ...

Haemorrhagic Bullous Myringitis This video shows a haemorrhagic blister arising from the right eardrum secondary to viral infection. It presents with earache and fullness sensation. Blood-stained serous discharge occurs following its rupture. The condition is self-limiting and treatment is symptomatic.

Linear IgA Dermatosis - Bullous Disease of Childhood Dr. Wendy Levinbook, MD discusses Linear IgA Dermatosis - Bullous Disease of Childhood. See more at PLEASE RATE AND COMMENT!!! Linear IgA disease (LAD) typically occurs after puberty with the majority of cases presenting after the age of 40. Chronic bullous disease of childhood (CBDC) usually presents before the age of 5. Both have a slight female predominance. Patients with LAD present with pruritic, annular, or grouped papules, vesicles, or bullae distributed symmetrically on extensor surfaces. The clinical presentation may be indistinguishable from that of dermatitis herpetiformis. Patients may also present with lesions that appear similar to those found in bullous pemphigoid or epidermolysis bullosa acquisita. Oral and conjunctival surfaces may be involved resembling cicatricial pemphigoid. Rarely systemic symptoms such as fever, arthritis, arthralgias, and malaise may occur. This disorder has been associated with the intake of many drugs including vancomycin, lithium, and diclofenac. These patients also demonstrate a small increased risk of lymphoid malignancy. In CBDC, young patients present with clustered, tense bullae, often on an inflammatory base giving a cluster of jewels appearance. Lesions are typically located in the perineum and perioral region. New lesions may appear around the periphery of previous lesions giving a giving the appearance of a collarette of blisters. The sensation of pruritus or burning is common. For both disorders, blister ...

Herpes Gestationis Dr. Wendy Levinbook, MD discusses Herpes Gestationis. See more at PLEASE RATE AND COMMENT!!! Herpes gestationis (HG) is a rare bullous dermatosis of pregnancy and the postpartum period. Disease onset is typically during the 4th to 7th months of pregnancy. However, it may occur during the 1st trimester or in the postpartum period. HG may or may not recur with subsequent pregnancies, but if it does, it typically begins earlier on in the pregnancy. Patients may also experience flares with the first few postpartum menses, with oral contraceptives, or with hormone-producing tumors. Clinically, lesions may present as red edematous papules, urticarial plaques, vesicles, large tense bullae, erosions, or crusts. Milder cases may present with only a few red papules or with isolated urticarial plaques. Lesions are typically located on the abdomen but they may spread to other areas. This condition is usually extremely pruritic. Mucosal surfaces tend to be spared. HG is an acquired autoimmune disorder that occurs secondary to the formation of IgG antibodies that interact with bullous pemphigoid antigen 2 (180 kDa hemidesmosomal transmembrane antigen, also known as type XVII collagen). Once deposited, these antibodies activate the complement cascade which in turn generates an inflammatory response and the cutaneous features of inflammation. Blister formation is in the lamina lucida on electron microscopic exam. Histopathologic evaluation reveals liquefaction ...

Video 4 - PKP for Pseudophakic Bullous Keratopathy.

Regurgitate - Effortless Regurgitation Of Bright Red Blood 1994 [PART 1] Regurgitate Effortless Regurgitation Of Bright Red Blood 1994 (1 - 12) : 1. Intro: The Act of Intestinal Regurgitation 2. Disgorging Foetus 3. Confluent Macular Drug Eruption 4. Bullous Impetigo 5. Fleshfeast 6. Anorectal Ulceration 7. Vulva Fermentation 8. Multicystic Kidney 9. Mucupurulent Offal Grinder 10. Total Dismemberment of a Female Corpse 11. Carnal Cacophony 12. Vomit Breath

Pemphigus Vulgaris Treatment Dr. Wendy Levinbook, MD discusses Pemphigus Vulgaris Treatment. See more at PLEASE RATE AND COMMENT!!! Therapy is aimed at reducing antibody synthesis. Unlike disorders such as bullous pemphigoid or dermatitis herpetiformis where there is a large inflammatory component in addition to the immune component, anti-inflammatory drugs have no known benefit in the treatment of pemphigus vulgaris. It is generally agreed that patients with only limited initial disease need as much intensive therapy to induce a remission as patients with extensive involvement. Prednisone is the standard initial therapy unless contraindicated. Most patients obtain a complete or almost complete clinical remission within 8 to 10 weeks and then the dose can be tapered gradually. Low doses are then maintained for several years. Other immunosuppressive drugs such as azathioprine or cyclophosphamide may be added if prednisone fails to induce a remission or if the patient develops serious corticosteroid complications. Mycophenolate mofetil, methotrexate, and cyclosporin are added to prednisone as adjuvant therapies less frequently. Other treatments that have been utilized include intravenous pulse methylprednisolone, intravenous pulse cyclophosphamide, adjuvant intravenous gammaglobulin, immunoablative intravenous cyclophasphamide without stem cell rescue, intramuscular gold, and extracorporeal photochemotherapy. Death formerly occurred in almost all cases. However, with the development of ...

Dr Luis Diaz pt 2 2010 JC Bystryn Pemphigus & Pemphigoid Meeting: From the Bench to the Bedside November 5-6, 2010 in Bethesda MD Diversity of the autoantibody response in pemphigus (IgM, IgE, IgG subclasses) A copy of the slides can be found at

Dr David Rubenstein pt 1 2010 JC Bystryn Pemphigus & Pemphigoid Meeting: From the Bench to the Bedside November 5-6, 2010 in Bethesda MD Human studies of blocking signaling pathways

Bullous Diseases Pathophysiology Dr. Wendy Levinbook, MD discusses Bullous Diseases Pathophysiology. See more at PLEASE RATE AND COMMENT!!! The basement membrane zone (dermal-epidermal junction) is continuous along the basal epidermal cells and consists of four compartments the basal cell plasma membrane, the lamina lucida, the lamina densa, and the sublamina densa. The basal cell plasma membrane contains hemidesmosomes which are located at regular intervals along the dermal surface of the plasma membrane of the basal keratinocytes. These anchor the epidermis, through connecting (anchoring) filaments to the lamina densa and ultimately to the underlying dermis. The hemidesmosomes also provide a site of attachment for the basal intermediate filaments, keratins 5 and 14. The hemidesmosomes consist of at least four protein components. Bullous pemphigoid antigen 1 (230 kD) and plectin are intracellular components. Bullous pemphigoid antigen 2 (180 kD, type XVII collagen) and alpha 6 beta 4 integrin are transmembrane components. The lamina lucida lies beneath the plasma membrane and separates the hemidesmosomes from the lamina densa. It is an electron lucent region that contains the anchoring filaments laminins 5, 6, and 7. These originate in the hemidesmosomes of the plasma membrane and insert into the lamina densa, thus connecting the basal keratinocyte plasma membrane to the lamina densa. The lamina densa lies beneath the lamina lucida. It is composed predominantly of type IV collagen ...

IPPF Advocacy Action and Support for Pemphigus and Pemphigoid Learn about pemphigus and the work that the IPPF does through the words of those it affects: patients, their families, and their doctors.

Paraneoplastic Pemphigus Dr. Wendy Levinbook, MD discusses Paraneoplastic Pemphigus. See more at PLEASE RATE AND COMMENT!!! Paraneoplastic pemphigus (PNP) typically affects middle-age patients but it can rarely occur in children. There is no racial or ethnic predilection and the incidence is equal in males and females. The most constant clinical feature of this disorder is intractable stomatitis consisting of erosions and ulceration of all surfaces of the oropharynx, including the lips. In fact, this may be the only disease manifestation. Other mucous membranes such as the conjunctival, esophageal, laryngeal, tracheobronchial, nasopharyngeal, oropharyngeal, vaginal, and penile mucosa may be involved. Cutaneous lesions are varied and can include tense bullae resembling bullous pemphigoid, erosions resembling pemphigus vulgaris, target lesions resembling erythema multiforme, lichenoid lesions resembling lichen pl***, or arcuate lesions resembling linear IgA dermatosis. Involvment of the palms and soles with bullae and lichenoid lesions is common and helps to distinguish PNP from other disorders. PNP is associated with either benign or malignant neoplasms in all cases. Non-hodgkin's lymphoma is the most commonly associated tumor. Histopathologic exam demonstrates features of both pemphigus vulgaris and erythema multiforme with suprabasilar acantholysis, basal cell vacuolization, dyskeratotic keratinocytes, and a lichenoid or perivascular mononuclear cell dermal infiltrate. Direct ...