Pemphigoid Gestationis Research Paper

Epidermolysis Bullosa is a genetic disorder that causes the skin to blister even with the slightest force. Epidermolysis Bullosa is found in three different types. Each are caused by different genetic mutations. The most common form of Epidermolysis Bullosa (EB) is Epidermolysis Bullosa simplex (EBS). The less common types of EB

1. A culture and sensitivity of pus draining from the right inguinal fold cystic sites was obtained today. Please follow up with culture results and treat as per culture results dictate.

The 2nd possibility would be PUPPP, which is pruritic urticarial papules and plaques of pregnancy. This typically is red and begins on the abdomen and then spreads to the extremities which is consistent with her history but it is unusual to also start this early in pregnancy.

defect in melanin that can be noticed to a skin and hair very clear in patients who have PKU.

Almost one-half of these patients had a disease type where pocks were sufficiently low in number to remain separated by normal skin. The rest of affected individuals developed more serious illness, where a larger number of lesions became confluent in certain areas.

Other lab tests can be considered, IgM, IgG for the diagnosis of Erythema in fectiosum, measles, rubella Pityriasis (tinea versicolor). Patch testing can be done to determine if the allergic dermatitis is present. In this case, patient will need to have referrals to dermatologist for patch testing. Antistreptolysin O titer or strep culture is helpful in the diagnosis of autoimmune disorder psoriasis.

Tinea pedis is diagnose on the patients foot by the symptoms, Or, a doctor may order a skin

L, et al.), Immunofluorescence mapping (IFM), Transmission electron microscopy (TEM), and mutation analysis. IFM and TEM are techniques that can both be used to assess the degree of skin cleavage. TEM was originally the standard for EB diagnosis until IFM. Examining for mutation is the first step because mutations across affected family members typically have equivalent mutations for dominant disorders, such mutations are the keratin 5, keratin 14, type VII collagen, and mutations found in those with EBS (Intong, LRA, and DF Murrell). EM allows for the imaging of particular skin ultrastructure of proteins that interact within basement membrane zone (BMZ), identifying microsplits and small changes in the dermo-epidermal junctions that can be indistinguishable by IFM. Specimens must be taken from a new blister and put on the correct media in order to get the proper diagnosis. However, TEM is expensive and must be done by experienced technicians and dermatopathologists and done in specialized laboratories. IFM is more accessible because it is less expensive and more responsive than TEM, it allows for the discovery of skin ultrastructure of proteins of the BMZ. Target proteins for EB are keratin 5 and 14, other subtypes of EB include the mutation of plectin, α6β4 integrin, dystonin, laminin-332, collagen

The first line of defense is formed by the stratum corneum, the uppermost layer of the epidermis. In the stratum corneum, filaggrin (FLG), a late epidermal differentiation protein, plays a pivotal role in the barrier function. It has been reported that loss of function variant of FLG gene leads to impaired skin barrier function and strong predisposing factor for atopic dermatitis (Palmer et al., 2006). FLG mutations may also increase the susceptibility to haptens, because mutations within the FLG gene were reported to represent a predisposition to contact allergy in both mice (Moniaga et al., 2010) and humans (de Jongh et al., 2008; Novak et al., 2008). On the other hand, other reports failed to find a clear association between contact allergy risk and FLG mutations (Lerbaek et al., 2007; Schnuch et al., 2010); therefore, further studies are needed to conclude the association between FLG mutation and contact dermatitis. Tight junctions are a second barrier to block antigen penetration into the skin. These junctions are composed of several proteins such as claudins and occludins in the stratum granulosum. Protein antigens are blocked from penetrating the body by this barrier. It has recently been reported that activated Langerhans cells (LCs) can elongate their dendrites above this barrier to take up protein antigens (Kubo et al., 2009), and the deficiency of LCs leads to reduced clinical

Skin: Warm, wet and sweaty (diaphoresis) but good colour. Diaphoresis is a common occurrence in patient with acute MI. No lesion, no nail clubbing and no cyanosis.

Symptoms usually include skin lesions paired with pain described as a burning sensation, along with itchiness and prickling sensations as well. One common symptom is very painful photosensitivity. This then manifests itself as a burning and itching sensation on the epidermal layer of the skin. At certain times, the itching sensations are completely unbearable. Rubbing the itchy spots with ice can be the only relief, and the relief only lasts for a short period of time. Regular anti-itch remedies, including cortisone anti-histamine topical preparations, and Calamine lotion generally provide little to no relief. Even exposal to surgical lights can trigger this itchy reaction. Prolonged exposure to the sun can lead to oedema of the hands, face (sometimes occurring on the lips), and feet; which rarely leads to blistering and petechiae (small red or purple spots appearing on the skin either in particular areas or widespread throughout the surface of the body). Also, skin thickening may occur, depending on the severity of EPP in the specific patient. When a person has EPP, their skin may appear red, dry and scaly. It looks as though the skin is raw but dry at the same time. The skin may also be scabbed

Dermographism is reported to occur in 25% -50% of healthy population among which 5% are symptomatic. Histamine is most likely a mediator, other mast cells such as prostaglandins, leukotrienes, platelet activating factor, serotonin , chemotactic factors are not directly related. It has been hypothesized that the IgE-sensitized mast cells can react to unknown antigen which is induced by skin stroking. H.Pylori have an etiologic role in dermographism.

PPE is characterized by multiple sharply demarcated urticarial papules that are either skin-colored or erythematous. The lesions are symmetrically distributed and more commonly seen on the extremities, but are also found on the trunk, face, or be generalized with sparing of mucous membranes, palms and soles, and digital web spaces. Studies have shown that 95% of lesions are located on the extremities, arms and legs, most frequently on the extensor surfaces and dorsum of the hands. PPE has a chronic course that waxes and wanes, and the lesions change appearance over time, with new lesions appearing daily. As the pruritus beings with lesion appearance, scratching leads to excoriations, secondary infections, and post-inflammatory hyperpigmentation, eventually leading to scarring and prurigo-like nodules. The lesions of PPE are predominantly papular, but there have been variants reported that display pustular lesions with acneform appearance.

[Adapted from Pan M, Liu X, Zheng J. The pathogenic role of autoantibodies in pemphigus vulgaris. Clin Ex. Dermatol 2011;36(7):703-07.]

The sign and symptoms of PPH include; the apparent excessive bleeding, hematocrit-reduction of the number of red blood cells, reduced blood pressure, development of symptoms of shock and anaemia, and severe pain and swelling of tissues and muscles of the vagina, vulva, pelvic and perineum (Simpson & Creehan, 2008). Besides, Ricci & Kyle (2009) avow that there are different factors that place a mother at risk for PPH, and they comprise; prolonged first, second or third stage of labour, previous history of PPH, foetal macrosomia, uterine infection, arrest of descent and multiple gestation. Other risk factors may include; mediolateral episiotomy, coagulation abnormalities, maternal hypertension, maternal exhaustion, malnutrition or anaemia, preeclampsia, precipitous birth, polyhydramnios and previous placenta previa (Ricci & Kyle, 2009).