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A scalp easily extracted show a hook-shaped appearance biopsy is done showing a dense lymphocytic infiltrate at the level of the isthmus. Frontal fibrosing alopecia telogen hairs, anagen hairs have a curled appearance at the root. The clinical scenario describes a patient with alopecia vellus hair-bearing areas in men and women areata. Testosterone binds the androgen receptor pecia, lymphocytic type, thought to be a variant of lichen planopilaris. The following hair shaft disorders are associated with woman with a bandlike area of hair loss along the fronincreased hair fragility and breakage: totemporal rim; loss of eyebrows is variably seen. Trichorrhexis nodosa active border of hair loss, there is perifollicular erythema ii. Hair shaf disorders are typically divided into those that cause increased fragility/breakage and those that do Answers not. In the case of idiopathic hirsutism, women will presinvaginata, and monilethrix typically present with short, ent with the clinical signs of androgen excess, however, broken hair. Clinical picture, histopathology, and approach to diagnosing hair shaft disorders. Fibrosis of palpebral conjunctiva develops secondary to chronic papillary conjunctivitis and irritation. Which of the following syndromes is associated with larization, and interstitial keratitis glaucoma Vitamin C (Ascorbic Acid) Deficiency A. All the following can be found in Vogt-Koyanagi Harada syndrome except: Questions A. What is the causative organism of Oculoglandular correlation, management, and follow-up in five patients. There are also reported families with leukonychia and acquired sensorineural deafness 4. If traumatic, phenol destruction of the lateral part of the nail plate emphasize nontraumatic nail practices and reduce leading to a narrowed nail. Concurrent use of topical anti-yeast mediand/or drainage of purulent collection may be cations can reduce colonization and hasten reattachnecessary ment. Treat underlying cause if to moist local environments or in patients who damage still active or related to an underlying disease the cuticle through traumatic nail practices. High-potency topical steroids for control of below); chronic cases: reduction of wetwork and condermatitis. Complete avoidance of acrylic nails and tact with irritants and discontinuation of traumatic nail glues should alleviate the problem, but underlynail practices is necessary. Short-term use of highing issues that prompted use of artificial nails will potency topical steroids. Oral antifungal medications should not be Genetic Syndromes used as single therapy, but have not been disproven as 1. The angle that the proximal nail fold makes with the proximal nail plate is called Lovibond Tumors of the Nail Area angle.

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In girls, this deceleration continues until the age of about 11 years, at which time the adolescent growth spurt begins. Growth and growth rate charts are readily available from the Centers for Disease Control and Prevention website. The predicted height can be compared with the present height percentile, and any significant deviation can be a clue to an abnormal growth pattern in a child. It is important to remember that some forms of growth hormone deficiency are inherited, so one should not automatically assume that the short child with short parents has familial short stature. When have most children achieved the height percentile that is consistent with parental height In a child with short stature, what rate of growth makes an endocrinologic cause unlikely In general, heights should be measured over at least a 6-month interval to calculate an accurate rate because growth rates are not completely linear, and measurement is relatively imprecise. Growth rates that are consistently below the 25th percentile or crossing percentiles downward after the age of 2 years warrant careful consideration and possibly investigation. When evaluating a short child, why should you ask when the parents reached puberty The age at which puberty occurred in other family members may help identify children with constitutional delay because this entity tends to run in families. Most women will remember their age at menarche, and this age can be used as a reference for the age at which other pubertal events occurred. The most useful reference point for adult males is the age at which they reached adult height because almost all normal males will have reached their adult height by the age of 17 years (before high school graduation). For children with an average growth rate, pubertal growth begins earlier in girls. Mean age at the initiation of this spurt is 11 years for boys and 9 years for girls. Girls generally stop growing at an average of 14 years of age, but boys continue to grow until 17 years of age. The timing of the pubertal growth spurt may be earlier in certain ethnic groups and in very obese children. Disproportionate short stature generally refers to an inappropriate ratio between truncal length and limb length (upper to lower segment ratio). Lower segment (limb length) is the distance from the superior border of the pubic bone to the floor surface. Height minus the lower segment gives the height of the upper segment (truncal length). In an infant, the head and trunk are quite long relative to the limbs, so the ratio of truncal length to limb length is about 1. Throughout childhood, this ratio declines, so that by 7 to 10 years of age this ratio is about 1. Extensive laboratory tests are generally not indicated unless the growth velocity is abnormally low. Depending on the ethnic background of the child or the clinical history, testing might also be done for celiac disease, inflammatory bowel disease, renal tubular acidosis, or other occult conditions. Random growth hormone levels are of little value because they are generally low in the daytime, even in children of average height. In a very obese child, how does height measurement help to determine whether an endocrinopathy might be the cause If the height of a child is at, or greater than, the mid-parental height percentile, an endocrine cause of the obesity is unlikely. In some children with craniopharyngiomas, significant obesity with good linear growth can be seen despite documented growth hormone deficiency. If an infant is demonstrating deceleration of a previously established growth pattern or growth that is consistently less than the fifth percentile, the pattern of growth of head circumference, height, and weight can help establish the likely cause (. There are three main types of impaired growth: n Type I: Retardation of weight with near-normal or slowly decelerating height and head circumference; most commonly seen in undernourished patients. How can one track growth in children who have spinal cord abnormalities or severe scoliosis There is an excellent 1:1 correlation between span (longest fingertip to longest fingertip measured across the nape of the neck) and height. Thus, span is a useful proxy measure for height/length if it is not possible to get an accurate height. Height and rate of growth, when determined in this way, can be plotted on standard growth and velocity charts. Standards of normal skeletal radiographic maturation are available, and these are based on the progression of ossification centers that occur at particular ages. This result can be compared with chronologic age to gauge the remaining potential for growth. The interpretation of bone ages can be somewhat difficult and dependent on the pediatric experience of the radiologist. A single bone age is of value for differentiating familial short stature and genetic diseases, in which bone age is normal, from other causes of short stature. In endocrine disease, the bone age falls progressively further behind the chronologic age. Bone age may be normal or delayed in patients with chronic disease, depending on the severity of disease, its duration, and the type of treatment used. Bone age is used as a diagnostic key: genetically determined short stature (bone age chronologic age) versus constitutional delay (bone age < chronologic age). Random growth hormone levels are usually not helpful (due to pulsatile delivery during sleep); provocative testing is more reliable. Short stature with overweight suggests endocrinopathy (adrenal, thyroid) and growth hormone deficiency. Growth hormone deficiency that appears during the first year of life is associated with hypoglycemia; after the age of 5 years, it is associated with short stature. If the results of history, physical examination, and clinical laboratory evaluation are unremarkable, the child is seen once every 3 to 6 months for accurate height measurements and determination of growth velocity. In patients with constitutional delay, the rate of bone maturation should keep pace with the chronologic age. In children who are of midto late pubertal ages (girls >13 years; boys >14 years) but showing minimal or no signs of puberty, selective use may be made of estrogen or testosterone supplementation to initiate puberty, or additional assessment may be indicated. Opponents argue that short stature is not a disease, that current height velocity may not be predictive, and that what constitutes growth hormone sufficiency and insufficiency is not clearly defined. Long-term safety remains under study, and some recent studies suggest impairment of testicular function in treated males. Proponents counter that the treatment is safe and does improve height in 50% of treated patients to at least 5 cm greater than pretreatment predictions. Surveys have indicated that most pediatric endocrinologists support growth hormone use in patients with short stature, normal growth hormone stimulation tests, and subnormal growth velocity. Hypogonadotropic hypogonadism and delayed puberty often coexist with growth hormone excess, and affected children exhibit eunuchoid body proportions. If the growth hormone excess occurs after puberty (after epiphyseal closure), the more typical features of acromegaly occur, including coarsening of the facial features and soft tissue swelling of the feet and hands. A serum glucose of less than 50 mg/100 mL is defined as hypoglycemia in childhood.

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The presenting clinical appearance varies from a white patch to a nonhealing ulcer to an exophytic lesion Histopathology ure 2-70). In the latter group is the clinically pathologic Most oral squamous cell carcinomas are moderately diferentity verrucous carcinoma. This subset of squamous cell entiated or well-diferentiated lesions ures 2-74 and carcinoma, sometimes associated with the use of smokeless 2-75). Keratin pearls and individual cell keratinization are tobacco, presents as a broad-based, wartlike mass. In H&E-stained sections of poorly diferentiated lesions, keratin is absent or is seen in minute amounts. However, it can be identifed using immunohistochemical techniques for the demonstration of antigenic determinants on otherwise occult keratin intermediate flaments. A signifcant infammatory host response is usually noted surrounding the nests of invading tumor cells. Rarely, an oral squamous cell carcinoma appears as a proliferation of spindle cells that may be mistaken for a sarcoma. Immunohistochemical staining can be used to identify keratin antigens in this lesion when H&E-stained sections show equivocal fndings ure 2-76). Verrucous carcinoma is characterized by very welldiferentiated epithelial cells that appear more hyperplastic than neoplastic. A key feature is the invasive nature of the lesion in the form of broad, pushing margins. The advancing front is usually surrounded by lymphocytes, plasma cells, and macrophages. Diagnosis based solely on microscopic features is often difcult; it is frequently necessary to consider the lesion in the context of clinical presentation. Papillary squamous cell carcinoma resembles verrucous carcinoma but is less diferentiated and has a poorer prognosis. This tumor may be confused microscopically with basaloid adenoid cystic carcinoma and adenosquamous carcinoma. Chronic trauma, including factitial carcinoma extension into salivary excretory ducts (sialadeor self-induced injury, may mimic squamous cell carcinotropism) can be regarded as a high-risk microscopic indinoma. Careful history taking is especially important, and cator of potential recurrence but does not necessarily defne biopsy fndings confrm the diagnosis. Considerable variation between tumors is seen contiguous tissues, midline granuloma and necrotizing sirelative to the numbers of mitoses, nuclear pleomorphism, alometaplasia would be serious diagnostic considerations. Treatment of resectable squamous cell carcinoma of the oral cavity is based on the location and stage of the primary tumor. As such, local surgery of the primary tumor, as well as regional surgery of the neck nodes, is considered and individually planned for each patient. Local surgery of the primary tumor must consider the removal of soft tissue and bone, as indicated. Removal of the cancer in soft tissue is referred to as a wide local excision, incorporating a 1. Mandibular resections are subclassifed as marginal resections whereby the inferior border of the mandible is General clinical experience with patients with squamous preserved, or as segmental resections whereby the full height cell carcinoma of the oral cavity shows that they most comof the mandible is sacrifced, thereby creating a defect in monly present with one of the four following clinical continuity of the mandible. B, Immunohistochemical stain for keratins showing positive staining of tumor cells. Typically, composite resections include a monobloc likely indicative of metastatic squamous cell carcinoma. The frst is when palmildly enlarged lymph nodes can be due to the incisional pable cervical lymphadenopathy exists. Identifcation of disseminated metastases might change a treatment plan from surgical to nonsurgical. The third, and most thought-provoking, indication for neck dissection is management of the neck when lymphadenopathy is not apparent. Occult neck disease is defned as cancer present in lymph nodes in the neck that cannot be palpated clinically and do not appear on special imaging studies. Numerous studies have examined the likelihood of occult neck disease as a function of the anatomic site of the primary cancer and as a function of its size and thickness. Tese studies clearly show that early squamous cell carcinoma of the oral tongue (T1-2, N0) may be associated with occult neck disease in nearly 40% of cases. This explains why many surgeons advocate performing a neck dissection for early squamous cell carcinoma of the tongue. The specimen Early disease of the foor of mouth (followed by disease of consists of a monobloc resection of the foor of mouth, mandible, and the buccal mucosa, maxillary gingiva, mandibular gingiva, ipsilateral neck nodes. Indications include midline primary cancers that are all of the aforementioned structures ure 2-81). By defmidline of the oral cavity and those cancers that cross the nition, then, the sternocleidomastoid muscle, internal jugumidline. Under such circumstances, the neck may be classilar vein, and spinal accessory nerve are intentionally prefed as bilateral N0 or ipsilateral N1 and contralateral N0. The supraomohyoid neck dissection, the most The bilateral N1 neck may also be encountered. This neck dissection, tralateral neck was performed, the rate of occult contralattherefore, is indicated in managing the N0 neck with a high eral neck metastasis was found to be 21% when ipsilateral likelihood of occult neck disease. When bilateral neck dissections are required in the manTese data point to the need to consider contralateral neck agement of patients with oral squamous cell carcinoma, surgery for patients in whom an ipsilateral N1 neck exists, maintenance of at least one internal jugular vein is required particularly when managing midline or bilateral primary to avoid intraoperative/postoperative complications such as cancers. Both are performed when patients present with palpable (N1) cervical lymphadenopathy. The internal jugular vein is noted on the medial aspect of the sternocleidomastoid muscle. The spinal accessory innervation of the trapezius muscle remains intact in this type of neck dissection. Unfortunately, despite numerous refnements in surgery Surgical management of squamous cell carcinoma ultiand radiation therapy, the 5-year survival rate for all pamately is based on decision making for optimal control of tients with squamous cell carcinoma (including all sites and local disease while existing or potential lymph node drainstages) has improved minimally in the past 50 years. The use of radiation therapy often plays a role in the sole management of squamous cell Radiotherapy Management of Squamous Cell carcinoma of the oral cavity, with or without chemotherapy, Carcinoma of the Oral Cavity or as an adjunct in the postoperative phase. Several investigational tracer compounds may have clinical application for head and neck cancers. A dental panoramic radiograph is obtained to assess both dental status and possible mandibular involvement of oral cavity tumors. Radiotherapy patients require a pretreatment dental consultation regardless of whether they are dentate or edentulous.

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Differential diagnosis Cells from a cervical adenocarcinoma should be differentiated from cells derived from a reparative epithelium, endometrial adenocarcinoma and extrauterine cancer. The reader is referred to Chapter 2 in this book for discussion and illustration of repair epithelial cells. In general, cells from an endometrial tumor are smaller than those of an endocervical cancer and they are usually associated with a large amount of necrotic debris. In difficult cases, a fractional uterine curettage should be done to distinguish these two lesions histologically. The reader is referred to Chapter 7 for discussion and illustrations of malignant endometrial cells. These malignant cells are, in most cases, found in a smear background that is free of necrotic debris and inflammatory exudate. In doubtful cases, clinical data and fractional curettages of the uterus would be of diagnostic help. The reader is referred to Chapter 6 for a more detailed discussion on extrauterine cancers. The diagnostic accuracy rate of invasive cervical adenocarcinomas in different reported series ranged from 86% to 97. The cytologic detection of cervical adenosquamous carcinomas appears to be more difficult leading to a false-negative rate up to 55%. Adenoma malignum and adenoid cystic carcinoma are rare occurrences in this location. Glassy cell carcinoma is a poorly differentiated adenosquamous cell carcinoma and accounts for 1% to 2% of all cervical cancers. In typical cases, the tumor yields in Pap smears single and clustered large malignant epithelial cells with oval nuclei and prominent nucleoli, similar to those of a nonkeratinizing squamous cell carcinoma. In other cases exfoliated tumor cells do not display a ground-glass cytoplasm and a firm diagnosis of glassy cell carcinoma can be only made by tissue biopsy. The tumor occurs mainly in elderly patients, but it may occur in patients under 50 years of age. The neoplasm commonly forms a polypoid friable mass and consists of small cancer cells forming clusters, cords and trabeculae with lumens containing hyaline eosinophilic material. It shows in Pap smears clusters of small cells with scant cytoplasm and small, oval, hyperchromatic nuclei. Tumor histology showing small tumor cells forming round spaces containing dense, hyaline eosinophilic material. Minimal deviation adenocarcinoma is a rare tumor accounting for about 1% of all primary cervical adenocarcinomas. Histologically, it may be divided into 3 types: cervical, endometrioid and non-specific. It is usually sporadic but it may rarely occur synchronously or precede an ovarian tumor that is commonly mucinous in nature. Due to diagnostic delay, this neoplasm is usually diagnosed at a high stage and therefore will have a poor prognosis. In about 50% of cases, foci of moderately or poorly differentiated adenocarcinoma are present. But a few more pleomorphic tumor cells with large, irregular nuclei and conspicuous nucleoli are present (C). This type of tumor exfoliates sheets of columnar glandular cells with low-grade oval nuclei in palisade at free borders. The 5 and 10-year survival rates of patients with clear cell carcinoma are 55% and 40%, respectively. Histologically, it is characterized by a papillary, microcystic, tubular or solid pattern. Villoglandular carcinoma is a rare cervical cancer with low-grade nuclei and an excellent prognosis. It is composed of epithelial papillae with thick fibrovascular cores and shows in Pap smears monolayered sheets of malignant epithelial cells with folding and nuclear crowding. The tumor is aggressive and has early pelvic and periaortic lymph node metastases. Histologically the tumor is characterized by the presence of thin fibrovascular cores and covered by pleomorphic malignant glandular cells with prominent nucleoli. Cytologic manifestations of advanced endometrial adenocarcinomas in cervical-vaginal smears. Cytologic diagnosis of adenocarcinoma in situ of the cervix uteri and related lesions. Expanded criteria for the diagnosis of adenocarcinoma in situ of the cervix and related lesions. Comparison with typical endometrial adenocarcinoma with villoglandular component and papillary serous carcinoma. Atypical glandular cells and endocervical adenocarcinoma in situ of the uterine cervix. Cytologic findings in minimal deviation adenocarcinoma (adenoma malignum) of the cervix. Cytologic examination to detect clear cell adenocarcinoma of the vagina and cervix. Exfoliative cytology of in situ and microinvasive adenocarcinoma of the uterine cervix. A frequent potential pitfall in the cytologic diagnosis of endocervical dysplasia on cervical smears. Minimal deviation endometrioid adenocarcinoma of the uterine cervix: a report of 3 cases with exfoliative cytology. Adenoid cystic basal cell carcinoma of the cervix: a potential pitfall in cervicovaginal cytology. Cytologic and biopsy findings leading to conization in adenocarcinoma in situ of the cervix. Exfoliative cytology of adenoma malignum (minimum deviation adenocarcinoma) of the uterine cervix. Histologically, these tumors are classified into 4 subtypes: typical and atypical carcinoid tumors, small cell carcinoma and large cell carcinoma with neuroendocrine differentiation. It is occasionally associated with Cushing syndrome or symptoms of other peptide hormones. The tumors are classified as homologous and heterologous depending on the nature of its stromal neoplastic cells. These neoplasms commonly exfoliate malignant glandular cells in Pap smears, and stromal tumor cells are usually not observed. Stromal cell sarcoma of the cervix is a very rare tumor that tends to occur in postmenopausal women (mean age, 54 years). Histologically it is characterized by malignant, uniform cells or slightly pleomorphic cells with scant cytoplasm. Other cervical nonepithelial cancers such as rhabdomyosarcoma, leiomyosarcoma, non-Hodgkin lymphoma, adenosarcoma, alveolar soft part sarcoma, granulocytic sarcoma are exceedingly rare tumors. Of these tumors, carcinomas of the breast, stomach and colon are the most common primaries while those arising from other anatomic sites such as the lung, pancreas, bladder, liver, kidney and gallbladder are rare. Regardless of the primary site, nearly 90% of women with metastasis to the cervix have evidence of a disseminated cancer, and the most common symptom is vaginal bleeding, occurring in 75% of patients. A metastatic moderately differentiated colonic adenocarcinoma yields abundant necrotic debris and malignant glandular cells with elongated nuclei in syncytial clusters and in irregular sheets with tumor cells in palisade at free borders. Metastatic mammary duct carcinoma to the cervix yields malignant glandular cells in clusters and in Indian file arrangement. A vaginal smear in this case may reveal tumor cells in irregular, tight tri-dimensional clusters. The presence of psammoma bodies should alert the observer to the possibility of a papillary serous ovarian carcinoma, and effort should be made to identify psammoma bodies surrounded by malignant epithelial cells to confirm the diagnosis. Cervicovaginal cytology in carcinosarcoma, malignant mixed mullerian tumor of the uterus. Primary cervical adenocarcinoma with intestinal differentiation and colonic carcinoma metastatic to cervix.

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Coma is a possible out to produce profound mood changes known as come of eclampsia, not an outcome of a hy glucocorticoid psychosis. Preeclampsia is the triad of hypertension, proteinuria, and edema seen in Answer A is incorrect. Eclampsia occurs when seizures fects of bleomycin are pulmonary fbrosis, skin accompany the symptoms of preeclampsia. Neural tube defects cin), Bleomycin, Vinblastine, and Dacarba are usually detected in utero by increased zine. Be Yolk sac tumors are the most common malig cause the patient may exsanguinate, ruptured nant testicular and ovarian tumors in children. Remember, tumor markers should not be used this patient does not have the symptoms of to make the primary diagnosis, but for confr a tubal pregnancy. These indices are con is also produced by pancreatic, gastric, and sistent with iron-defciency anemia. The marker for mela is caused by either vitamin B12 or folate def noma is S-100. Hepatomas volume suggests a normocytic, normochromic are not known to elevate S-100 levels. This marker also is el increased, sideroblastic anemia should be sus evated with lung and gastric cancers. The marker for pros (Hct, hemoglobin) are consistent with anemia, tatic carcinoma is prostate-specifc antigen. This vignette suggests on immunofxation, coupled with the pre a hepatoma (hepatocellular carcinoma), which dominance of plasma cells in the bone marrow is associated with an elevated a-fetoprotein biopsy, are consistent of Waldenstrom macro level. Other risk emia is a B-lymphocyte lymphoproliferative factors include Wilson disease, hemochroma disorder that often results in a syndrome of tosis, alcoholic cirrhosis, a1-antitrypsin def blood hyperviscosity secondary to increased ciency, and exposure to toxins and carcinogens levels of IgM (both heavy and light chains), such as afatoxin. Yolk sac tumors (also known as en row biopsy reveals diffuse infltrates of lym dodermal sinus tumors) arise from the germ phocytes, plasma cells, and intermediate cells that eventually become the adult gonads. The patient in this vignette, on the other Waldenstrom macroglobulinemia often pre hand, has normal calcium levels. High levels sent with similar abnormalities to those listed of monoclonal Ig chain, usually IgG or IgA, (mild anemia, blood urea nitrogen on the up are secreted into the serum. Ig light chains, per limit of normal, and increased total pro known as Bence-Jones proteins, are often se tein). They experience a variety of signs and creted in the urine, leading to renal failure. In symptoms such as constitutional symptoms, this patient, immunofxation shows high levels episodic bleeding, lymphadenopathy, and hep of IgM, which is consistent with Waldenstrom atosplenomegaly. Heavy-chain disease plasma cells that secrete abnormal immuno encompasses a number of disorders including globulins containing light chains (usually ) chronic lymphocytic leukemia/small lympho that deposit in various tissues. Bone marrow bi cytic lymphoma, lymphoplasmacytic lym opsy may show normal bone marrow or a mod phoma, and Mediterranean lymphoma. The est increase in the number of plasma cells with common feature of these disorders is that they pale pink amorphous deposits and increased secrete free heavy-chain fragments. Al Congo red staining and apple green birefrin though the image depicts lymphoplasmacytic gence by polarizing microscopy. One per lymphatic drainage from the testes, therefore, cent of cases progress to a symptomatic mono is to the para-aortic lymph nodes in the lumbar clonal gammopathy (eg, multiple myeloma). The deep inguinal from myeloma by the lack of lytic lesions and nodes drain the vessels in the spongy urethra little to no plasmacytosis. External iliac nodes It can also spread to lymph nodes and other ex drain the bladder. Gluteal lymph nodes replacement of normal marrow cells with ab drain the deep tissue of the buttocks. Although multiple itself, but not of the testes, may spread to the myeloma can also demonstrate similar bone superfcial inguinal lymph nodes. The scro marrow biopsy fndings as Waldenstrom mac tum is an outpouching of abdominal skin, and roglobulinemia, multiple myeloma is not as drainage of this skin is to the superfcial ingui sociated with hyperviscosity syndrome. This patient has tu retinal hemangiomas can rupture, leading to berous sclerosis, an autosomal dominant dis retinal detachment. Sun sensitivity would which regulate cellular growth and differen be associated with xeroderma pigmentosum, tiation. Typical skin fndings include the ash-leaf develop basal cell and squamous cell carcino spot, Shagreen patch, and facial angiofbro mas of the skin. Patients with neurofbromatosis type 1 have body, and coagulation factors and platelets are characteristic cafe-au-lait spots, cutaneous consumed actively. The active conversion of f neurofbromas, and Lisch nodules in the iris, brinogen to fbrin as part of the convergence of along with central nervous system tumors such both clotting cascades leads to decreased levels as optic gliomas and astrocytomas. At the same time, anticoagula with neurofbromatosis type 2 have bilateral tion factors such as plasmin and protein C are acoustic neuromas as a characteristic fnding, being activated, leading to fbrinolysis and in and may present with bilateral tinnitus and creased levels of D-dimers in the circulation. More fore, a decrease in the levels of fbrinogen males than females are affected, with symp would be expected. The overgrowth of blood vessels leads to angiomas and hemangioblastomas in Answer E is incorrect. Patients also show one of the factors involved with the extrinsic cystic growths in the kidneys and pancreas, pathway. Busulfan used to be a and interfere with the absorption and synthesis treatment in patients intolerant of hydroxy of this vitamin. Like the others, it has now been sup other conditions related to fat malabsorption planted by imatinib. Hydroxyurea is mod veloped and the liver reserves of vitamin K are erately effective in bringing the disease un small. Vitamin K defciency usually presents der control and maintaining a normal white with bleeding diathesis, hematuria, melena, count, but its use has been superseded by ima bleeding gums, and ecchymoses. The most common the treatment of choice for this condition but tumor of the parotid gland is the pleomorphic has been superseded by imatinib. On histopathology, gen from binding and interfering with platelet it is characterized by the presence of multiple aggregation. It is used in acute coronary syn cell types, classically epithelial cells in a chon drome and angioplasty. This translocation generates a monoamine oxidase B inhibitor that causes an fusion protein, Bcr-Abl, that functions as a con increase in the availability of dopamine. It is stitutively active tyrosine kinase, promoting used with levodopa in the treatment of Parkin dysregulated cell growth and division. Platelet phospholipids are derlies Bernard-Soulier disease, an inherited required for both the intrinsic and extrinsic disorder in platelet adhesion due to the ab clotting pathways. Periph bind to platelet phospholipids, thereby making eral blood smear may show increased platelet them accessible to clotting factors and leading size (macrothrombocythemia) but no schis to recurrent venous and arterial thrombosis. Their presence would cause bleeding hemolysis, neurologic symptoms, and renal in rather than thrombus formation. However, laboratory fndings include a decreased platelet count Answer B is incorrect. This patient has no history of heparin X-linked disorder leading to defciency of fac exposure. This answer describes the abnormality underlying von Willebrand Answer E is incorrect. A mild anemia will be present, but the intervals for the remainder of their lives. Bisphosphonates such fcient a-globin chains for normal HbA1 lev as alendronate and risedronate are used to treat els. Deletion of only a single a-gene results in multiple myeloma, which is known to cause an asymptomatic carrier with no hematologic bone destruction as a result of increased os manifestations. Bisphosphonates have been shown to decrease pain and fractures in mul Answer C is incorrect. Glucose-6-phosphate vincristine and vinblastine are microtubule in dehydrogenase defciency does not present hibitors used to treat some cancers, including with an abnormal Hb electrophoresis. The abnormal normal monoclonal serum immunoglobu Hb molecule (HbH) contains four b-chains, lin level but no other signs of malignancy and is detected by electrophoresis. Hb Bart is the most inherited diseases involving decreased syn severe of the hemoglobinopathies, involving thesis or complete absence of either the deletion of all four a-globin genes.

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The very nature of this technique guarantees the exclusion of false positives, since the algorithms are based on the recognition of unique isotopic patterns. Up-to-date metabolomics techni ques include hundreds of compounds identiable in a single experiment, with direct links and crossed information that facil itates the understanding of the roles of these small molecules in the landscape of a metabolic pathway. This approach consists in a proling tech nique based on a unique isotopic signature per metabolite recognized by a mathematical algorithm embedded in Clustern der Software. Internal standards are obtained by using 95% and 5% 13 C abundance metabolites offered in different conceptual experi ments, which are specically designed to the object of study. Reproducibility is achieved by running the rst and spiking the samples with an internal standard and it is very easily identiable by the software, which confers a validation of the library component. The internal standard that complements the set and is spiked in the samples is chemically equal to the reference library (. Aqueous humor is a nourishing uid that contains amino acids, glucose, ascorbic acid, and other small molecules and removes metabolic products, sustaining the cornea and the lens. One of the vital functions of the aqueous humor is maintaining the intraocular pressure, and, therefore, changes in the metabolomics composition of aqueous humor could derive in serious ocular pathologies [3]. The samples are rst treated with a methanol, acetonitrile, and acetone mix for extraction purposes. The matrix is run at the beginning of the sequence in both modes and every ten samples to create a daily library. The internal standard is run by itself in both modes previously to the run of the samples as well. Reconstitute the sample as follows: (a) Prepare a mixture of methanol and water 2%. This way, by creating a personal library with the on-site instrument in a consistent manner, it is possible to create the best matching system to analyze and quantify the samples with the same instrument. It is extremely important not to forget to run the library every ten samples to create a reliable library, this is a critical step of the whole process. Not all the samples are the same, from tissue to cells, the nature of the sample varies enormously the concentration of the meta bolites. Cayuela A, Liu Y, Mandal R, Neveu V, Pon A, Accessed 17 Oct 2018 Knox C, Wilson M, Manach C, Scalbert A 3. Key words Cell culture, Cell counting, Fluorescence-based lipid transport assay, Immunocytochem istry, Lipidomics, Metabolites, Mass spectrometry, Lipids, Lipid extraction 1 Introduction Lipids are biological molecules that comprise the cytoplasmic back bone of cells, are involved in molecular transport, and play a crucial role in cell signaling [1]. Progress in biophysics, chemistry, and genetics has attracted novel attention toward the various biological roles that membrane lipids serve [2]. The plasma membrane and internal organelles of eukaryotic cells constitute an interconnected membrane system that conserves distinct components [3]. The trafficking of proteins from their site of synthesis to their nal destinations has been extensively studied. Most lipid synthesis occurs within the cytosolic leaet of the endoplasmic reticulum, and in order to reach the unique organelle lipid compositions observed in eukaryotes, certain mechanisms must be present to direct specic lipid species to different cellular membranes [4]. Following the attachment of lipids to their target sites, lipids are irregularly distributed between the extracellular and Sanjoy K. Three cate gories of proteins have been described that function in the assembly and termination of membrane asymmetry: ippases, oppases, and scramblases [6]. Here, we propose several methods for determining transport of lipid metabolites across trabecular meshwork cells, a representative model for cells of presudo-endothelial origin. One method of studying lipid metabolite transport is to attach a uorescent head group to the lipids of interest, which enables determination of lipid transport kinetics and the subsequent localization into the cellular compartments [9]. This method relies on the assumption that addition of the uorescent head group does not cause the entire molecule to change. However, one limitation is that once a uores cent head group is added to the lipid, the molecule fundamentally changes chemically. Following the transport of the lipid molecule into the cell, the head group could potentially become modied. Therefore, the transport of the head group is not necessarily the transport of the lipid. Nevertheless, this method provides a simpli ed way of determining the transport kinetics and localization of the lipid. The assessment of kinetic parameters and determination of localization among other characteristics complemented with molecular biology will aid in identication of molecular transpor ters in cell types related to pseudo-endothelial cells. A second method of studying lipid metabolite transport is through the imple mentation of mass spectrometry. Advances in mass spectrometry have generated exhaustive developments in holistic, high sensitivity, and high-throughput lipid analysis [2]. This method is based on the assumption that in the time frame, the lipids are being examined, and they are not modied, so that the mass by charge ratio remains consistent. This will generate viable, oating cells that can be utilized for cell counting, uorescence assay, and immunocytochemistry. Place a coverslip in the center of the hemocytometer to guide the insertion of the solution into two respective wells. Observe the center of the hemocytometer where the two wells meet under a compound light microscope at 20A magnica tion until a grid is clearly visible. Include any cells inside the box as well as the cells touch ing the left line and top line of the box. Calculate the number of viable cells per milliliter with the following equation: Viable count live cells per milliliter Number of live cells counted= Number of large corner squares counted A2 A 1=Volume of large square in milliliters 3. Allow the tubes to sit at room temperature with the uorescent lipid for the desired times. Following the completion of incubation time for the rst set of four, centrifuge the tubes for 5 min at 1600 A g so that a pellet forms. Aspirate the supernatant for the three uorescent lipid tubes, leaving 20 L of solution in each of the vials. Add the distinct uorescent lipid solutions to the rst three wells on the plate in the same row. Analyze uorescence via the plate reader at a gain, excitation, and emission that are recommended for the uorescent lipid being investigated. Following the uorescence assay, add a volume equivalent to cytochemistry 3000 cells to a poly-D-lysine-coated coverslip in a petri dish that will represent each respective time point (Note 4. Following incubation, ensure under a light microscope that the cells are properly adhered. Apply nail polish around the edges of the coverslip to seal, and let it dry for 20 min. Add 200 L of chloroform to create the 1:1 solvent methanol to chloroform solution. All sam ples in glass vials must rst be transferred before being inserted into the centrifuge machine. There will now be an upper (aqueous) and lower (lipid) fraction within the samples. Place samples in speed vacuum, and ensure that all samples are Removal placed in a balanced manner. Afterward, Spectrometry Analysis the samples are run with and without the standards for quantica tion purposes. Dilute each standard to the desired concentration, typically Samples and Lipid 10 pmol/L, in a mix of methanol and chloroform (1:1). To obtain a spectra for every parameter, run a solvent aliquot and note the consistently abundant peaks. To ensure homogeneity of the trypan blue dye with the trabe cular meshwork cells, it is advisable to gently ick the side of the microcentrifuge tube as this will not disrupt the trabecular meshwork cells. Following centrifugation, it is important to note that the pellet may not be visible. It is best to leave at least 20 L of solution at the bottom of the microcentrifuge tube so the pellet does not become aspirated along with the supernatant. It is also feasible to leave the cells overnight to adhere to the poly-D-lysine-coated coverslips; however, 4 h is sufficient for proper adherence.

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To help detect a consumptive coagulopathy, Investigations a coagulation screen, including measurement of brinoThe most common cause of purpura is trauma, espegen and brin degradation products, may be necessary. The bleeding time, and a Hess tourniquet test for capWhen purpura has no obvious cause, investigations illary fragility, help less often. Skin biopsy will conrm should include a platelet count, prothrombin time, a small vessel vasculitis, if the purpura is palpable. The Infected pompholyx primary forms are developmental defects, although Lymphatic obstruction Filariasis signs may only appear in early puberty or even in Granuloma inguinale adulthood. Tumour Lymphatic destruction Surgery Treatment Radiation therapy Tumour Elevation, graduated compression bandages and stockings (p. If erysipelas recurs, long-term penicillin tongue and lymphoedema of lip) should be given. Surgery occasionally helps to remove Yellow nail syndrome an obstruction or restore drainage. Lymphangitis this streptococcal infection of the lymphatics may Treatment occur without any lymphoedema. Penicillin ucloxacillin, cephalexin levant blood constituents may be needed initially. The glands themselves are multilobed and contain Cause cells full of lipid, which are shed whole (holocrine secretion) during secretion so that sebum contains Acne vulgaris their remnants in a complex mixture of triglycerides, fatty acids, wax esters, squalene and cholesterol. Furthermore, sebum Androgenic hormones, especially dihydrotestosexcretion often remains high long after the acne has terone, stimulate sebaceous gland activity. Androgens (from the testes, ovaries and hydroxysteroid dehydrogenase, which convert weaker adrenals) are the main stimulants of sebum excretion, androgens to dihydrotestosterone, which in turn binds although other hormones. In acne, nal androgens for a short time after birth, and then the sebaceous glands respond excessively to what are lie dormant until puberty when a surge of androgens usually normal levels of these hormones (increased produces a sudden increase in sebum excretion and target organ sensitivity). Fifty per cent of females with acne have slightly raised free testosAcne terone levelsausually because of a low level of sex Acne is a disorder of the pilosebaceous apparatus hormone binding globulin rather than a high total characterized by comedones, papules, pustules, cysts testosteroneabut this is still only a fraction of the and scars. Rupture of these follicles is associated with intense inammation and tissue damage, mediated by oxygen free radicals and enzymes such as elastase, released by white cells. It colonizes the pilosebaceous ducts, breaks down triglycerides releasing free fatty acids, produces substances chemotactic for inammatory cells and induces the ductal epithelium to secrete pro-inammatory cytokines. There is a high concordance of the sebum excretion rate and acne in monozygotic, but not dizygotic, twins. Corticosteroids, androgenic and anabolic steroids, gonadotrophins, oral contraceptives, lithium, iodides, bromides, antituberculosis and anticonvulsant therapy can all cause an acneiform rash. Heat and humidity are responsible for this variant, which affects Caucasoids with a tendency to acne. Presentation Common type Lesions are conned to the face, shoulders, upper chest and back. Open comedones (blackheads), because of the plugging by keratin and sebum of the pilosebaceous orice, or closed comedones (whiteheads), caused by overgrowth of the follicle openings by surrounding epithelium, are always seen. Depressed or hypertrophic scarring and postinammatory hyperpigmentation can follow. On resolution, it leaves deeply pitted or hypertrophic scars, sometimes joined by keloidal bridges. Although hyperpigmentation is usually transient, it can persist, particularly in those with an already dark skin. Psychological depression is common in persistent acne, which need not necessarily be severe. Tars, chlorinated hydrocarbons, oils, and oily cosmetics can cause or exacerbate acne. Suspicion should be raised if the distribution is odd or if comedones predominate (. Glucose intolerance, dyslipidaemia when acne, dominated by papulo-pustules rather than and hypertension may be other features. Hyperpigmentacoincides with the prescription of a drug known to tion, ambiguous genitalia, history of salt-wasting in cause acneiform lesions (see above). Some athletes still childhood, and a Jewish background, are all clues to use anabolic steroids to enhance their performance. Congenital adrenal hyperplasia is associated with high levels of 17-hydroxyprogesterone, and androgensecreting tumours with high androgen levels. Pelvic ultrasound may reveal multiple small ovarian cysts, although some acne patients have ovarian cysts without biochemical evidence of the polycystic ovarian syndrome. Differential diagnosis Rosacea (see below) affects older individuals; comedones are absent; the papules and pustules occur only on the face; and the rash has an erythematous. Pseudofolliculitis barbae, caused onset of virilization (clitoromegaly, deepening of voice, by ingrowing hairs, occurs on the necks of men with breast atrophy, male pattern balding and hirsutism) curly facial hair and clears up if shaving is stopped. An optimistic of patients, but some 5% of women and 1% of men approach is essential, and regular encouragement still need treatment in their thirties or even forties. Occasionally an underlying cause (see above) is found; this should be removed or treated. Investigations At some time most teenagers try antiacne preparaNone are usually necessary. Cultures are occasionally tions bought from their pharmacist; local treatment is needed to exclude a pyogenic infection, an anaerobic enough for most patients with comedo-papular acne, infection or Gram-negative folliculitis. Only a few although both local and systemic treatment are needed laboratories routinely culture P. Any acne, including infantile acne, which is associLocal treatment (Formulary 1, p. Benzoyl peroxide bleaches also anti-inammatory and inhibits the formation coloured materials, particularly towels and annels. It should be applied twice daily, but not (tretinoin, adapalene, tazarotene) normalize follicular used for more than 6 months at a time. Patients should be warned about skin largely been replaced by topical retinoids as aggressirritation (start with small amounts) and photosensitive scrubbing can rupture comedones. Tretinoin can be prescribed as a lotion, containing sulphur are available on both sides of the cream or gel. The weakest preparation cin, erythromycin and sulfacetamide (Formulary 1, should be used rst, and applied overnight on alternp. Some combinations work better than to be stopped temporarily because of irritation. Erythromycin with benzoyl peroxide, it may be worth increasing the combined with a zinc acetate complex (Formulary 1, strength of tretinoin after 6 weeks if it has been well p. The combination of benzoyl peroxide in the icrobial, an inhibitor of 5reductase (see above), morning and tretinoin at night has many advocates. It appears to work inium chloride, used as antiperspirants, may help quicker and to be tolerated better than tretinoin. Cover-ups help some patifound in one study to be more effective than tretinoin ents, especially females, whose scarring is unsightly. The antibiotic should not be used for less than treatment (Dianette: 2 mg cyproterone acetate and 3 months and may be needed for a year or two, or 0. It should be taken on an empty stomach, countries and may help persistent acne in women. Even with long courses, serious side-effects are A triphasic pill, or a pill with a high oestrogen rare, although candidal vulvovaginitis may force a content, is best for women with acne who also require change to a narrower spectrum antibiotic such as oral contraception. Absorption is not signicantly Isotretinoin (13-cis-retinoic acid, Formulary 2, p. Minocycline is much more this is an oral retinoid, which inhibits sebum excrelipophilic than oxytetracycline and so probably contion, the growth of P. The drug is reserved for severe nodulologically more effective than oxytetracycline and cystic acne, unresponsive to the measures outlined tetracycline and, unlike erythromycin, little resistance above.

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The most common injuries to suspect are lumbar spine injuries, particularly a flexion disruption (Chance) fracture and bowel or bladder perforations or disruptions. In a 7-year-old boy with a radiographically proven pelvic fracture, what diagnostic procedure should be done The urethra, as it passes through the prostate, is very close to the pubic bone and is thus susceptible to injury from a pelvic fracture. Urethral damage should be suspected in all patients with pelvic fractures, even those without hematuria. A boggy, high-riding prostate found on rectal examination and blood seen at the urethral meatus are clinical signs of possible urethral disruption; these two findings are contraindications for passing a Foley catheter. A partial urethral disruption could potentially be made into a complete one with the passing of the catheter. It is used as a screen for abdominal bleeding as blood appears black (hypoechoic) against the bright (hyperechoic) background of the internal organs. This noninvasive tool provides clinicians with rapid information about potentially life-threatening thoracic and abdominal injury. Lavelle and Fred Henretig that were retained from previous editions of Pediatric Secrets. Can clinical clues suggest that adrenal insufficiency is a primary rather than secondary problem Furthermore, in secondary insufficiency, the zona glomerulosaof the adrenal gland (responsible for aldosterone secretion) remains intact. Therefore, hyperkalemia and volume depletion are distinctlyuncommon, butdilutionalhyponatremiamayoccurasaresultofdecreasedcapacityto excrete a water load. Depending on the enzyme involved, the blockade can result in excesses or deficiencies in the other steroid pathways. There are substantial differences in prevalence in various racial and ethnic groups. A late-onset or attenuated form (mild deficiency) manifests in adolescent girls with hirsutism and menstrual irregularities. In boys, androgen excess does not cause any clearly abnormal appearance of the external genitalia. Because 50% to 60% of oral hydrocortisone is absorbed, the recommended oral physiologic replacement is about 12 to 15 mg/m2 per 24 hours. Hence, when the term stress dose is used, it generally means that the dose is at least three times above physiologic replacement, that is, 50 to 100 mg/m2 per 24 hours of hydrocortisone. Doses of glucocorticoid higher than 50 mg/m2 per 24 hours of hydrocortisone that are being used to treat these conditions are referred to as pharmacologic doses; that is, the medication is not being used for adrenal replacement or stress dosing. When does adrenal-pituitary axis suppression occur in prolonged glucocorticoid treatment As a general rule, the longer the duration of treatment and the higher the dose of glucocorticoid, the greater the risk for adrenal suppression. If pharmacologic doses of glucocorticoids are used for less than 10 days, there is a relatively low risk for permanent adrenal insufficiency, whereas daily use for more than 30 days carries a high risk for prolonged or permanent adrenal suppression. The reason for glucocorticoid treatment must also be considered; that is, a child with severe head trauma may have initially been on treatment with glucocorticoids to reduce brain swelling but is also at significant risk for secondary pituitary deficiencies. Hyperparathyroidism: n Familial n Isolated n Syndromic Idiopathic: n Williams syndrome Infantile: n Subcutaneous fat necrosis n Secondary to maternal hypoparathyroidism Infection: n Tuberculosis Infiltration: n Malignancy n Sarcoidosis Ingestion: n Milk-alkali syndrome n Thiazide diuretics n Vitamin A intoxication n Vitamin D intoxication Skeletal disorders: n Hypophosphatasia n Immobilization n Skeletal dysplasias 12. An 8-year-old in a spica cast after hip surgery develops vomiting and a serum calcium concentration of 15. A serum calcium concentration of more than 15 mg/dL or the presence of significant symptoms. Meticulous monitoring of input and output and of serum and urinary electrolytes (including serum magnesium) is vital. Additional treatment with glucocorticoids and antihypercalcemic agents may also be needed. Serious consideration should be given to intensive care unit treatment and careful monitoring of inputs and outputs. An easy way to remember the difference is that the Chvostek sign affects part of the cheek. Hypoparathyroidism can result from anomalies of the gland, destruction by surgery or autoimmune processes, biosynthetic abnormalities, or decreased distal cellular responsiveness to the hormone. Additionally, intestinal absorption of calcium is decreased, urinary losses of cholecalciferolbinding globulin are increased, and urinary losses of calcium are increased with prednisone therapy. In older children, it may occur in the context of autoimmune polyglandular disease or mitochondrial myopathy syndromes. Nausea, vomiting, irritability, personality changes, progressive obtundation, and seizures can result. An individual with hyponatremia that has developed over a prolonged period of time is less likely to have symptoms than one in whom the hyponatremia has developed acutely. Urine osmolality elevated compared with serum osmolality (a urine osmolality <100 mOsm/dL usually excludes the diagnosis) 3. Urinary sodium concentration excessive for the extent of hyponatremia (usually >20 mEq/L) 4. The infant may present with symptoms of failure to thrive as a result of chronic dehydration, or there may be a history of repeated episodes of hospitalizations for dehydration. Often, caretakers report a large-volume intake or an inability to keep a dry diaper on the infant. In the older child, the reappearance of enuresis, increasing frequency of urination, nocturia, or dramatic increases in fluid intake may heraldthe diagnosis. Deprivation of water intake for a limited time and judicious monitoring of physical and biochemical parameters may be required. This is a state of severe metabolic derangement that results from both insulin deficiency and increased amounts of counterregulatory hormones (catecholamines, glucagon, cortisol, and growth hormone). Its main features are hyperglycemia (glucose usually >300 mg/dL), ketonemia (serum ketones >3 mmol/L with ketonuria), and acidosis (venous pH <7. The concern is that too rapid a rehydration with falling osmolarity might contribute to edema. Because the severity of dehydration is often difficult to accurately assess, fluid is usually infused at a rate rarely in excess of 1. Next 4 to 6 hours: Initiation of deficit fluid replacement continued with isotonic saline (or Ringer lactate) Thereafter: Change to a solution with tonicity >0. As a general rule, the serum sodium is low at the outset and rises throughout the course of treatment. An initial sodium of more than 145 mEq/L suggests severe dehydration or hyperosmolarity. If the patient is hypokalemic, potassium should be begun with the initial volume expansion and before insulin administration. Insulin administration results in potassium transport into cells with a further decrease in serum levels. If the initial potassium level is within a normal range, begin potassium replacement (with the concentration in the infusate at 40 mEq/L) after the initial volume expansion and concurrent with starting insulin therapy. If the initial potassium measurement is elevated, defer potassium replacement until urine output has been documented or the hyperkalemia abates. A low K is particularly worrisome because it suggests severe potassium depletion.

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The tumour cells from the underlying ductal carcinoma is found more frequently in children and has a better have migrated up into the lactiferous ducts and invaded the prognosis. Grossly, the skin of the carcinoma of the breast is a clinical entity and does not nipple and areola is crusted, fissured and ulcerated with constitute a histological type. The term has been used for oozing of serosanguineous fluid from the erosions breast cancers in which there is redness, oedema, tenderness (. B, There are clefts in the epidermal layers containing large tumour cells (arrow). In addition, the underlying breast contains invasive or non-invasive duct carcinoma which shows no obvious direct invasion of the skin of nipple. The breast cancers are subdivided into various histologic grades depending upon Figure 25. It is based on Ki-67) or by flow cytometry have a worse prognosis than 3 features: purely diploid tumours. Later, however, distant spread by lymphatic route to on the number and level of lymph nodes involved by internal mammary lymphatics, mediastinal lymph nodes, metastasis. More the number of regional lymph nodes supraclavicular lymph nodes, pleural lymph nodes and involved, worse is the survival rate. Breast is one iii) Fibroadenoma is a long-term risk factor (after over 20 years) of the most suspected source of inapparent primary for invasive breast cancer, the risk being about twice carcinoma in women presenting with metastatic carcinoma. Following factors act as Based on current knowledge gained by breast cancer determinants: screening programmes in the West employing mammo i) Ductal carcinoma in situ (comedo and non-comedo graphy and stereotactic biopsy, various breast cancer risk subtypes) is diagnosed on the basis of three histologic factors and prognostic factors have been described. Comedo type of in situ carcinoma has higher increased risk than women of the same age. Prognostic and predictive factors A summary combining all these factors is given in for invasive breast cancer have been extensively studied by Table 25. In addition, the skin is concerned with thermoregulation, conservation and excretion of fluid, sensory perception and, of course, has aesthetic role for appearance of the indidivdual. In general, it is composed of 2 layers, the epidermis and the dermis, which are separated by an irregular border. Cone-shaped dermal papillae extend upward into the epidermis forming peg-like rete ridges of the epidermis. The basal cell layer consists of a single layer of keratinocytes that forms by desmosomes. Interspersed in the keratinocytes are the junction between the epidermis and dermis. The nuclei melanocytes, a type of dendritic cells, seen as every tenth cell of these cells are perpendicular to the epidermal basement in the basal layer. These are hyperchromatic and normally contain cytoplasm containing melanin pigment granules that a few mitoses indicating that the superficial epidermal layers determines the appearance of an individual. The other type of ted with each other and with the overlying squamous cells dendritic cells in the basal layer are Langerhans cells which are bone marrow-derived cells of mononuclear-phagocyte system. This layer is composed of several layers of polygonal prickle cells or squamous cells. The layers become flat as they near the surface so that their long axis appears parallel to the skin surface. This layer is present exclusively in palms and soles as a thin homogeneous, eosinophilic, non nucleate zone. Intraepidermal nerve endings are present in the form of and connective tissue components. When the muscle or papillary dermis, and the deeper pars reticularis or reticular contracts, the hair becomes more erect, the follicle is dragged dermis. The dermis is composed of fibrocollagenic tissue upwards so as to become prominent on the surface of the containing blood vessels, lymphatics and nerves. The specialised nerve endings present at some sites the stratum corneum that develop at specially modified perform specific functions. The nail is composed of Pacinian corpuscles concerned with pressure are present clear horny cells, resembling stratum lucidum but are much in the deep layer of skin. Meissner corpuscles are touch receptors, located in the papillae of skin of palms, soles, tips of fingers and toes. Before describing pathology of common skin diseases, the End-bulbs of Krause are cold receptors found in the external following pathologic terms in common use need to be defined genitalia. They are present all over the skin but are Dyskeratosis: Abnormal development of epidermal cells most numerous on the palms, soles and axillae. They are resulting in rounded cells devoid of their prickles and having coiled tubular glands lying deep in the dermis. Dyskeratosis is a feature of premalignant pass through the epidermis on the surface of the skin as pores and malignant lesions and is rarely seen in benign conditions. Apocrine glands are encountered in progress to vesicle formation in the epidermis. A few common examples of each glands are found everywhere on the skin except on the palms of these groups are described below. They are often found in association with hair but can be seen in a few areas devoid of hair as modified I. It Histologically, the characteristic feature is association of has, therefore, an intracutaneous portion present in the hair hyperkeratosis with thin or absent granular layer. The hair follicle consists of epithelial 770 Sex-linked ichthyosis is a sex-(X) linked recessive prone to develop infections, especially of lungs, and disorder. Histologically, the papillary dermis shows numerous Histologically, there is hyperkeratosis with normal or dilated blood vessels. The condition occurs as both autosomal dominant and autosomal A very large number of skin diseases have acute or chronic recessive forms. This is an autosomal the skin from outside or from within the body such as recessive disorder in which sun-exposed skin is more chemicals and drugs, hypersensitivity to various antigens vulnerable to damage. Many idiopathic varieties of skin disorders basal cell carcinoma and melanocarcinoma. In thinning and atrophy of stratum malpighii, chronic general, these conditions are clinically characterised by inflammatory cell infiltrate in the dermis and irregular itching, erythema with oedema, oozing and scaling. Changes However, irrespective of the clinical type of dermatitis, the of skin cancers mentioned above may be present in histopathologic picture is similar. In typical cases, there is extensive spongiosis (intercellular oedema) that may lead to forma papular eruption. The vesicles and bullae as well as the oedematous epidermis are permeated Histologically, the characteristic changes are hyper by acute inflammatory cells. The epidermis shows moderate acanthosis and homogeneous dyskeratotic material) and there is varying degree of parakeratosis in the horny layer with appearance of suprabasal clefts containing acantholytic formation of surface crusts containing degenerated cells. Urticaria pigmentosa may Chronic dermatitis shows hyperkeratosis, parakera occur as congenital form or may appear without any family tosis and acanthosis with elongation of the rete ridges and history in the adolescents. The upper dermis shows perivascular chronic inflammatory infiltrate and fibrosis Histologically, the epidermis is normal except for an (.

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Female sex hormones likely modify Basement membrane this pigmentation because women (especially those taking birth control pills) are more commonly afected than men. Note dendritic proThe amount of smoking that brings this condition on varies cesses of melanocyte and melanin transfer to keratinocytes. Clinical Features The anterior labial gingiva is the region most typically afected, where brownish color can vary from subtle to obvious. In India, the use of smokeless tobacco forms has been linked to oral melanosis, particularly among alcoholics. In smoking-associated melanosis, the intensity of pigmentation is time and dose related ure 5-4). Histopathology Melanocytes show increased melanin production, as evidenced by pigmentation of adjacent basal keratinocytes. Treatment With cessation of smoking, improvement can be expected over the course of months to a few years. Melanin is found within surrounding basal keratinocytes and subjacent connective tissue macrophages (termed melanophages). However, it may potentially mask other lesions or may be cosmetically objectionable. In cases where surface irregularity or focally intense pigment deposits are noted, biopsy should be performed. Melanotic macules have been described as occurring predominantly on the vermilion of the lips and gingiva, although they may appear on any mucosal surface. This mutation is inherited in an autosomal-dominant manner, and in addition to ephelides or melanotic macules, intestinal polyposis is present. Tese polyps are regarded as hamartomas without, or with very limited, neoplastic potential. They are usually found in the small intestine (jejunum) and may produce signs and symptoms of abdominal pain, rectal bleeding, and diarrhea. Histopathology Microscopically, melanotic macules are characterized by melanin accumulation in basal keratinocytes and normal numbers of melanocytes ure 5-9). Melanophagocytosis (melanin present within connective tissue macrophages) is typically seen within the lamina propria. Diferential Diagnosis B Tese oral pigmentations must be diferentiated from early superfcial melanomas. Oral A biopsy may be required to establish a defnitive diagnosis freckles and larger melanotic macules occur with generalof this lesion. Other presenting signs and symptoms of this syndrome include weakness, weight loss, nausea, Cafe-au-Lait Macules vomiting, and hypotension. Cafe-au-lait macules are discrete melanin-pigmented Pigmented macules have been described in association patches of skin that have irregular margins and a uniform with three other rare syndromes. Pigmentation of Physiologic (ethnic) pigmentation the conjunctiva and penis has been described in patients with Melanotic macule this syndrome. A rare condition, Bandler syndrome, may Smoking-associated melanosis feature melanotic macules of the oral mucosa and perioral Syndrome-associated pigmentation Peutz-Jeghers syndrome region together with hemangiomas of the small intestine. Tese lesions are characteristiMelanocytic nevus cally seen in older patients and appear as brown patches that Melanoma Amalgam tattoo are larger and darker than ephelides. The lesions are benign Drug-induced pigmentation but may be cosmetically objectionable, in which case they may be treated with cryotherapy or laser vaporization. This sporadic disorder is considered to be Neurofbromatosis strongly associated with mutation of the Gsa gene. Variants Neurofbromas of skin, oral mucosa, jaws have been associated with primary biliary cirrhosis and alopeCafe-au-lait macules of skin McCune-Albright syndrome cia. They generally show excess amounts of melanin in basal keratinocytes and subjacent macrophages. Melanocytes are normal in appearance and may be slightly increased a syndrome (Box 5-4). Although some overlapping nocytes and nevus cells, these cells have their origin in the features are known, the two conditions are distinct clinineural crest. Radiographs show for the neurofbromin protein that downregulates the funcan ill-defned lucency that may contain developing teeth. Variably sized nests of round to oval lesion of various cell types or tissue types. Generally, howcells are found within a well-defned connective tissue marever, nevus (or mole) used without a modifer refers to a gin. Cells located centrally within the neoplastic nests are pigmented lesion composed of nevus or melanocytic cells. Melanocytic nevi are collections of nevus cells that are Diferential Diagnosis round or polygonal and are typically seen in a nested patFew other lesions are reported in this age group and in this tern ure 5-13). Odontogenic cysts and the neural crest to the epithelium and dermis (submucosa), tumors would not be seriously considered in a diferential or to result from altered resident melanocytes. Clinical Features Treatment and Prognosis Melanocytic nevi of the skin are common acquired papular this lesion has been treated with wide local surgical excision lesions that usually appear shortly after birth and throughwith good results. Intraoral melanocytic nevi are relatively rare recorded; thus, close clinical follow-up after excision is reclesions that may occur at any age. Must differentiate from melanoma (biopsy) Types (in order of frequency): Intramucosal nevus Blue nevus Compound nevus Junctional nevus Probably has no malignant potential A mucosa, gingiva, alveolar ridge, and vermilion (Box 5-5; Figures 5-14 and 5-15). Histopathology Microscopically, several subtypes are recognized ures 5-16 and 5-17). Malignant transformation of an oral benign melanocytic nevus is highly improbable. Various observations support this statement, including (1) malignant features are never seen in oral nevi, (2) oral melanomas rarely, if ever, contain preexisting nevi histologically, and (3) almost no cases of the malignant counterpart of the relatively common oral blue nevus have been reported. Because oral melanocytic nevi can mimic melanoma clinically, all undiagnosed pigmented lesions should undergo a biopsy. In the oral cavity, intramucosal nevi are the most commonly seen variety, and blue nevi are the second most common. The so-called dysplastic nevus that is commonly seen in skin has not been observed in oral mucous membranes. Diferential Diagnosis Other clinical considerations that should be included with any type of oral melanocytic nevus are melanotic macule, amalgam tattoo, and melanoma.

References:

  • https://www.medrxiv.org/content/10.1101/2020.01.25.19014803v1.full.pdf
  • https://dphhs.mt.gov/Portals/85/dsd/documents/DDP/MedicalDirector/NauseaandVomiting.pdf
  • https://www.jpsr.pharmainfo.in/Documents/Volumes/vol9Issue01/jpsr09011712.pdf
  • https://cda-adc.ca/jcda/vol-75/issue-7/533.pdf

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