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للأسف , سمعت بهالحكي من رفقاتنا اللي راقبوكم بالامتحان ,
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أخي simply red مبروك العلامة

بالفعل كانت صدمة قصة انو الأسئلة كتابة وليست اتمتة
انا كمان قدمت جلدية
بشكل عام السلايدات كانوا سهلين بس سلايد الشرث زعجني كتير كتبتو رينو وما قبلوا الدكتور مع انو القصة ما كانت مفرقة كتيير بين الاثنين ومع هيك العلاج متشابه و ما حسبلي جواب العلاج صح
هيك انظلمنا لانو لو كان اتمتة كان انحسب الجواب صح

على العموم الحمد لله اجتني 28 / 30

موفق بالنظري

ألف مبروك عزيزي maxcool.....
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محربا جميعا...
ممكن أسأل حدا إذا في عندو دورة تشرين 2007
أو دورة الفصل الأول اللي قدمها طلاب الرابعة 2008
و لكم جزيل الشكر

مرحبا جميعا...
ممكن أسأل حدا إذا في عندو دورة تشرين 2007
أو دورة الفصل الأول اللي قدمها طلاب الرابعة 2008
و لكم جزيل الشكر

بس حبيت ذكر اذا حدا توفرت عندو هي الدورات يا ريت قلنا لانو الفحص قرب

ركز علي الاشياء COMMON وارجو الاستفادة من هدا الموضوع:
Epidemiology and clinical manifestations of leishmaniasis ]
INTRODUCTION — Leishmaniasis, caused by a heterogeneous group of protozoan parasites belonging to the genus Leishmania, results in a variety of different clinical syndromes. The classification and taxonomy of the organisms are confusing; several different approaches can be used: Leishmaniasis can be classified geographically into New World versus Old World disease. Infection can be divided into cutaneous, mucocutaneous, or visceral disease. Separation into subgenus, complexes, and species can be based upon taxonomy.
Specific organisms are often associated with a typical clinical picture. However, considerable overlap exists, and the relationship between the clinical syndromes and the different species is not always distinct. As an example, some Leishmania species are primarily dermatotrophic, while others are mainly viscerotropic. It has become increasingly clear that some species frequently associated with visceral leishmaniasis can produce skin lesions, and conversely, species usually found in the skin can disseminate viscerally. In addition, each clinical syndrome can be produced by multiple species. Thus, generalizations and classification can be difficult ( 1).
The epidemiology and clinical manifestations of leishmaniasis will be reviewed here, primarily using a syndromic approach to avoid the complicated taxonomy. Diagnosis and treatment issues are discussed separatelly
EPIDEMIOLOGY — Leishmania organisms are endemic in scattered foci in more than 80 countries on every continent except Australia and Antarctica. The overall prevalence of leishmaniasis is estimated to be 12 million cases worldwide, and the global yearly incidence of all clinical forms approaches 2 million new cases [1]. More than 20 Leishmania species have been identified. Most species cause disease predominantly in animals; humans become infected incidentally when they enter endemic areas. Although leishmaniasis occurs predominantly in individuals living in endemic regions, travelers to these areas can also be infected, even after less than one week of exposure
In addition, cutaneous leishmaniasis has reported in United States military personnel, primarily among those stationed in Iraq [7,30]. From August 2002 through April 2004 the Department of Defense reported 522 parasitologically confirmed cases of cutaneous leishmaniasis acquired in Iraq. Most infections were acquired near the borders of Iraq with Syria or Iran. All the 176 typed isolates were L. major. Approximately 75 percent of the lesions presented between August and September 2003, with further lesions peaking in presentation in September and October 2003.
The affected patients had a median of three lesions (range one to nine), with a diameter ranging from 3 to 40 mm. Most were on the arms or legs. The lesions were painless, centrally ulcerated, and peripherally indurated and erythematous. (See "Skin lesions in the returning traveler").
Sandfly vectors — Leishmaniasis is spread by the bite of a female sandfly. Sandflies of the species Lutzomyia serve as the vector in the New World, while the Phlebotomus species transmit infection in the Old World. Most sandflies typically bite at dusk, but certain vector species in parts of South America preferentially feed during daylight hours instead. Rodents and/or canines (wild or domestic) serve as the reservoir for most Leishmania species. However, in India and Bangladesh, L. donovani has no animal reservoir. Humans serve as both the natural reservoir and the host for infection in these countries.
Infection due to leishmaniasis occurs as a consequence of the interaction between the mammalian reservoirs, the sandfly vectors and humans. The disease is rural in some geographic areas and periurban or urban in others. Sandflies have a short flying range and thus must live close to animal reservoirs for perpetuation of transmission.
The mechanism of transmission from sandflies to humans is becoming better understood. In infected sandflies, the anterior midgut is blocked by parasite-derived promastigote secretory gel [8]. This blockade results in difficulty in feeding, resulting in multiple and longer feeding attempts and therefore a greater likelihood of transmission. In addition, both the gel and sandfly saliva, which are regurgitated with the metacyclic promastigotes during a bite, promote establishment of the parasite in the human host with exacerbation of the infection (see "Life cycle" below). The main active component in the gel is filamentous proteophosphoglycan.
Transmission to humans — Cutaneous and visceral disease can both have epidemic or endemic transmission patterns. Outbreaks tend to occur when susceptible hosts move into an area of endemic transmission or when a sandfly habitat is disturbed, such as with encroachment of settlements into forest areas .Both visceral and cutaneous leishmaniasis are increasing in prevalence globally because of urbanization, increases in rodent populations, decreased insecticide use, ecological changes resulting from war, and increased numbers of immunosuppressed and susceptible hosts
In addition to the usual means of transmission by the sandfly vector, disseminated forms of leishmaniasis can also be spread via shared needles, blood transfusions, vertically from the mother to fetus, or sexually [3].
LIFE CYCLE — Leishmania exist in nature in two morphologic states. They reside as intracellular pathogens within macrophages of mammalian hosts and as extracellular promastigotes within the gut of their sandfly vectors.
During the bite of a sandfly, flagellated metacyclic promastigote forms of the parasite are injected into the skin [10]. They are taken up by local tissue macrophages, within which the parasites transform into intracellular amastigotes [11]. Amastigotes multiply within the phagolysosomes of the macrophages. Infected macrophages either remain in the skin and cause cutaneous disease or disseminate throughout the reticuloendothelial system producing disseminated disease. The site of inoculation is often inapparent, but a small papule may form. In cutaneous syndromes, this papule grows and ulcerates to become the site of the lesion. By contrast, a local ulcer rarely develops in visceral syndromes.
If an uninfected sandfly bites an infected host, it takes up amastigotes residing within macrophages. These transform back into metacyclic promastigotes within the sandfly gut over a period of 4 to 14 days. They then migrate to the proboscis, the mouth part of the insect, thereby completing the life cycle.
CLINICAL SYNDROMES — Most infections with Leishmania are asymptomatic. The wide spectrum of disease that can be caused by Leishmania relates to intrinsic differences or differing virulence in the various parasite species, and genetic factors and differing immune responses of the host. When symptoms do occur, they can begin as soon as 7 to 10 days after exposure or be delayed by many years.
Leishmaniasis can be thought of as a spectrum of illness in similar terms to leprosy. (See "Overview of leprosy"). At one end, oligoparasitic disease associated with a marked cellular immune response (mucocutaneous leishmaniasis, post kala-azar dermal leishmaniasis, and leishmaniasis recidivans) At the other end, polyparasitic disease with macrophage predominance and no granulomatous inflammation (visceral leishmaniasis and diffuse cutaneous leishmaniasis) In the middle, intermediate forms (localized cutaneous leishmaniasis and viscerotropic infection)
Hosts who are malnourished or immunocompromised are more likely to have a high parasite burden and to develop symptoms.
Cutaneous syndromes — It is estimated that 1 to 1.5 million cases of cutaneous leishmaniasis occur annually; however, many more cases are not reported. More than 90 percent occur in Saudi Arabia, Iran, Afghanistan, Brazil, and Peru.
Cutaneous leishmaniasis is caused by organisms from the L. mexicana and L. braziliensis complexes, and by three ungrouped species, L. tropica, L. major and L. aethiopica. The typical incubation period between the time of the bite and clinical manifestations is one week to several months [12].
The cutaneous syndromes associated with Leishmania parasites include localized cutaneous leishmaniasis (LCL), mucosal leishmaniasis (ML), leishmania recidivans (LR), and diffuse cutaneous leishmaniasis (DCL).
Localized cutaneous leishmaniasis — Cutaneous lesions tend to occur on exposed areas of skin, beginning as a red papule that enlarges to form an ulcer with granulomatous tissue at the base and raised, heaped up margins (show picture 1). There is usually no surrounding induration. The ulcers are characteristically painless unless secondarily infected. Localized adenopathy may develop, especially in the early stages of the infection. Some individuals have multiple lesions, and lesions may occur in the distribution of lymphatic drainage. Nodular, psoriasiform, and verrucous forms arise less commonly.
LCL lesions typically undergo spontaneous resolution. The pace of this resolution varies according to the infecting Leishmania species and the immune reaction of the host. A residual hypopigmented, depressed scar at the site is common following cure.
The two main causes of LCL in the Old World are L. major and L. tropica. L. aethiopica can also cause localized cutaneous lesions; L. infantum, which is usually associated with visceral infection, occasionally provokes nodular skin lesions. In the New World, cutaneous lesions are caused predominantly by L. braziliensis, L. peruviana, L. guyanensis, L. panamensis, L. mexicana, and L. amazonensis. L. chagasi, which is typically associated with visceral leishmaniasis, also can have cutaneous manifestations, analogous to L. infantum.
There are some classic distinguishing clinical features between the Old and New World forms of cutaneous leishmaniasis. Old World cutaneous leishmaniasis typically has the following appearance, depending upon the inciting species: L. major tends to cause an exudative, "pizza-like" or "wet ulcer". The ulcer usually has a raised outer border, a granulating base, and an overlying white purulent exudate. After a typically short incubation period of one week to two months, the ulcer frequently grows to a size up to 6 cm in diameter over a short time period. Spontaneous healing typically also occurs quickly, usually within six months. Multiple lesions are common. L. tropica tends to evolve more slowly. It has a typical incubation period of two months to two years, and the ulcer does not usually grow larger than 1 to 2 cm. This ulcer is characterized as a "dry ulcer" because it usually has a central crust and no exudate. There may be satellite lesions, although single lesions are characteristic. Spontaneous resolution, when it occurs, happens more slowly, often taking one to two years. L. tropica can be associated with LR. L. aethiopica usually develops as a solitary lesion on the face with or without surrounding satellite papules that coalesce into spreading nodules or plaques. Lesions may spread along mucocutaneous margins but do not involve oral or nasal mucosa. These lesions typically show little inflammation and are more chronic than those seen with other Leishmania species, resolving slowly over many years. L. aethiopica can be associated with diffuse cutaneous leishmaniasis. L. infantum is usually associated with visceral leishmaniasis but can also be a cause of indolent, slow-growing nodular cutaneous lesions that can persist for years.
The lesions of New World cutaneous leishmaniasis tend to be difficult to distinguish by the etiologic leishmanial species. However, some classic features of certain species have been described. Primary lesions of L. braziliensis tend to be large, frequently with associated regional lymphadenopathy. A sporotrichoid pattern of multiple ulcers or subcutaneous nodules along the distribution of lymphatic drainage is common. The lymphadenopathy may appear prior to the development of an ulcer and may be accompanied by fever and malaise. Ulcers often heal within six months but may persist for one year or more. L. braziliensis can be associated with ML. L. mexicana generally produces small chronic ulcers, usually with only one or a few lesions. These tend to heal rapidly and spontaneously, often within three to four months. Lesions frequently occur on the ear, which relates to the biting habit of the vector. These lesions are referred to as "Chiclero's ulcers". L. mexicana and L. amazonensis can also be associated with DCL.
Leishmaniasis recidivans — LR refers to an uncommon syndrome caused by L. tropica infections in the Middle East. Following healing of the primary lesion, a few persistent organisms can cause new papules to form around the margins of the scar. These papules can ulcerate, heal, and reappear over decades. Thus, this syndrome is characterized by new lesions in the same area as an old scar, or by slowly] enlarging lesions that heal in the center. Patients tend to have a good cellular immune response, and few parasites are present in the lesion. A recent report described a patient who developed recurrence of LR 43 years after their initial symptoms [13].
Diffuse cutaneous leishmaniasis — Diffuse cutaneous leishmaniasis is a rare, syndrome that
الباقي في رسالة اخري].

باقي النص:

diffuse cutaneous leish :syndrome that
occurs mainly with L. aethiopica, L. mexicana, and L. amazonensis. The primary lesion does not ulcerate; rather
amastigotes progressively disseminate to macrophages in other areas of skin. Patients with DCL usually have a defect in the cell mediated immune response and are anergic. Nodules or plaques form typically occur on the face and cooler extensor surfaces of the limbs.
DCL characteristically follows a relapsing or chronically progressive course. Generalized skin nodules can develop over months to years, leading to marked deformity. These lesions may be mistaken for lepromatous leprosy. It is unclear if treatment of nonhealing lesions caused by these species helps to avoid late DCL.
Mucosal leishmaniasis — Mucocutaneous leishmaniasis (ML) only occurs in the New World and is mainly associated with L. braziliensis infection. Eleven cases of mucocutaneous disease were reported in travelers between 2003 and 2005; half of these cases were acquired in the Amazon region of Bolivia [14].
Months or years after resolution of the primary cutaneous lesion, recurrence at a distal mucosal site can follow due to hematogenous or lymphatic dissemination. This is also known as "espundia". It has been estimated that the lifetime risk of developing a mucosal lesion is 1 to 5 percent after a primary L. braziliensis lesion. Approximately 50 percent of the mucosal lesions occur in the first two to three years after the primary ulcer, and the rest occur decades later.
ML is associated with erosive disease of mucosal surfaces, most commonly of the nose, nasal septum, or mouth. However, other mucosal areas can be involved, including the cheek, pharynx, palate, epiglottis, larynx, vocal cords, trachea, and genitalia. Ulceration of the nasal septum can lead to septal perforation. The palate can also be destroyed. Patients may present with bleeding of mucosal surfaces.
Disease is classified as mild if the patient presents with nasal stuffiness alone, moderate if there is associated odynophagia or dysphonia, or severe if there is severe dysphonia or respiratory distress. Substantial disfigurement can result from destruction of the nasal cartilage and surrounding tissues. Aspiration and death can ultimately develop on rare occasions.
Visceral syndromes — The most common visceral syndrome is visceral leishmaniasis. Viscerotropic leishmaniasis caused by L. tropica and post kala-azar dermal leishmaniasis (PKDL) due to L. donovani also occur.
Visceral leishmaniasis (kala azar) — Visceral leishmaniasis (VL, also known as kala azar or black fever) is caused by the three parasite species of the L. donovani complex: L. donovani, L. infantum, and L. chagasi. Infections with these organisms are often asymptomatic or very mild, but in a minority of individuals there is progression to severe symptomatic disease known as kala-azar or black fever. This is associated with spread of the infection throughout the reticuloendothelial system. Studies in Brazil, for example, have shown that 7.5 percent of children are infected with L. chagasi each year, but only 1 of every 8 to 10 of these children develops symptomatic disease [15,16]. Similar figures have been reported from Kenya [17].
It is estimated that there are 500,000 new cases of symptomatic VL each year, resulting in up to 5000 deaths annually. More than 90 percent of the cases are reported from Bangladesh, India, Sudan, and Brazil, where there have been epidemics over the past 10 years. The peak age for developing symptoms from VL varies in different geographic regions [11]. L. infantum and L. chagasi typically affect children below the age of 10 years. However, VL due to these species can also occur in immunosuppressed adults, such as transplant recipients and patients receiving immunosuppressive chemotherapy [18]. L. donovani typically manifests in adolescence or young adulthood. The average incubation period is four to six months but can be as short as 10 days or be delayed by more than three years [12].
Human immunodeficiency virus (HIV) infection has altered the epidemiology of VL. In certain endemic areas of southern Europe, up to 30 percent of healthy young adults have a positive skin test indicating prior infection with L. infantum; these individuals usually remain asymptomatic [11]. However, there is a high incidence of coinfection with HIV in these areas, particularly in Spain, southern France and Italy, especially in injection drug users (IDU) [19,20]. Even in the era of potent antiretroviral therapy, VL is the fourth most common AIDS-related infection in Spain [21].
Since an intact cellular immune system is required to control leishmaniasis, individuals infected with HIV are prone to more severe clinical manifestations of leishmaniasis, whether the infection is new or reactivated [22]. In these regions where both infections are common, it is estimated that up to 70 percent of adult cases of VL are now associated with HIV, and that up to 10 percent of patients with AIDS present with VL as an opportunistic infection. Visceral disease is more common in patients with CD4 counts less than 300 cells/µL; disseminated disease occurs when the CD4 count is less than 50 cells/µL [23] As noted above, L. donovani infection also has a unique epidemiology in India. (See "Sandfly vectors" above). Humans serve as the reservoir for an anthrophilic sandfly vector; thus, transmission requires only infected humans and an appropriate vector. This differs from the usual situation where VL disease transmission also requires contact with an animal \reservoir. As a consequence, epidemics of infection occur more frequently in India.
VL caused by all three species has five characteristic hallmark features: Organomegaly Fever Cachexia Pancytopenia Hypergammaglobulinemai
Most patients do not recall a primary skin lesion
The characteristic symptoms in VL are fever and weight loss. The onset of disease can be insidious or acute. Examination often reveals massive splenomegaly and moderate hepatomegaly, with or without icterus. Lymphadenopathy is found in some patients, particularly in Africa.
Skin manifestations in VL are frequent. Kala-azar means "black sickness" and refers to the earth-gray skin color that is common in infected individuals, especially in India. Diffuse nodular skin lesions may also be present. Mucosal lesions consisting of oral or nasal ulcers may accompany the systemic illness, particularly in patients in the Sudan. Thrombocytopenia results in petechiae, ecchymoses, and gingival bleeding.
As the disease progresses, gastrointestinal (GI) involvement develops, resulting in diarrhea, malabsorption, hypoalbuminemia, peripheral edema, cachexia, and debilitation. Immune compromise secondary to neutropenia ultimately occurs, and bacterial superinfections are common. One study found that more than 60 percent of individuals developed bacterial infections late in their disease course; Pseudomonas aeruginosa and Staphylococcus aureus were common pathogens [24]. Tuberculosis or viral infections, such as measles, can also supervene.
Immunosuppressed individuals with VL, particularly HIV-infected patients, usually have clinical features similar to classic disease but can also have involvement of other organs and can present with unusual features. Extensive GI involvement with parasites in the rectal, jejunal, duodenal, gastric, and esophageal mucosa can occur, leading to symptoms such as dysphagia, odynophagia, severe watery diarrhea, intestinal hemorrhage, and rectal pain [25,26]. Splenomegaly may be absent. Immunocompromised patients may also develop diffuse papular skin lesions, and involvement of the central nervous system, larynx and lungs. Pulmonary involvement may lead to pleural effusions and pulmonary nodules. Aplastic anemia has also been described.
Viscerotropic leishmaniasis — Viscerotropic leishmaniasis is caused by L. tropica infection. This syndrome was first recognized in American troops stationed in the Persian Gulf in Saudi Arabia during Operation Desert Storm [27,28]. Typical symptoms in these troops included fever, chronic fatigue, malaise, cough, intermittent diarrhea, and abdominal pain that began up to seven months after leaving the endemic area. Examination often revealed adenopathy or mild, transient hepatosplenomegaly, but cutaneous ulcers typical of L. tropica were not evident. The diagnosis was established by bone marrow aspiration or lymph-node biopsy showing intracellular amastigotes. L. tropica was isolated by culturing these tissues. Serology was usually negative or of low titer in these individuals [28]. Patients generally responded to treatment with sodium stibogluconate. (See "Treatment and prevention of leishmaniasis").
Post kala-azar dermal leishmaniasis — Post kala-azar dermal leishmaniasis (PKDL) is a syndrome that can develop after treatment of generalized African or Indian visceral disease due to L. donovani. Different clinical pictures are seen in the two geographic locations [29]. Both cause a generalized cutaneous rash that is often papular or nodular and that can resemble leprosy. Severe forms with desquamation of skin and mucosae can occasionally be seen. Despite similar skin findings, each has varying prognostic features. In the African form, PKDL is typically seen during or at the end of treatment. A transient crop of papules appears over the face and arms in up to 50 percent of individuals, probably related to an immune response secondary to parasites in the skin. These lesions resolve over a few months and do not necessitate any further therapy. In the Indian PKDL syndrome, lesions typically appear insidiously two or more years after therapy has been completed. The lesions can be of varying forms, including hypopigmented macules, nodules, verrucous, or papillomatous growths. Lesions tend to be slowly progressive and seldom resolve without further therapy
T

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