liver FNA
everything above diaphragm, and gender related organs stain cytokeratin 7
below diaphragm, such as colon stain cytokeratin 20
not clear cut for pancreas, spleen, etc.
false positives may appear when enzymes from mitochondria react with peroxidase or if cells have many lysosomes
TTF-1 should stain nuclei since it is transcription factor
cirrhosis - replacement of normal architecture with nodule regeneration
fibrosis - may still have normal parenchyma
benign lymph node should not look monotonous, should have small/medium/large lymphocytes
CSF acellular or 1 or 2 cells
cryptococcus present in infection, reproduce by budding
stain with mucicarmine stain
breast cytology
LCIS may have small monotonous looking cells
medullary have very high grade looking cells
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Pneumocystis pneumonia (PCP) is a form of pneumonia caused by the yeast-like fungal microorganism Pneumocystis jirovecii (Jirovecii is pronounced "yee row vet zee eye"). The causal agent was originally described as a protozoan and spelled P. jiroveci and prior to then was formerly classified as a form of Pneumocystis carinii, a name still in common usage. These names are discussed below. As a result, Pneumocystis pneumonia (PCP) has also been known as Pneumocystis jiroveci[i] pneumonia and as Pneumocystis carinii pneumonia, as is also explained below.
Symptoms
Symptoms of PCP include fever, non-productive cough, shortness of breath (especially on exertion), weight loss and night sweats. There is usually not a large amount of sputum with PCP unless the patient has an additional bacterial infection. The fungus can invade other visceral organs, such as the liver, spleen and kidney, but only in a minority of cases.
[edit] Pathophysiology
The risk of pneumonia due to Pneumocystis jirovecii increases when CD4 levels are less than 200 cells/mm³. In these immunosuppressed individuals the manifestations of the infection are highly variable.[11] The disease attacks the interstitial, fibrous tissue of the lungs, with marked thickening of the alveolar septa and alveoli and leading to significant hypoxia which can be fatal if not treated aggressively; ergo, LDH levels increase and gas exchange is compromised. Oxygen is less able to diffuse into the blood, leading to hypoxia. Hypoxia, along with high arterial carbon dioxide (CO2) levels, stimulates ventilation, thereby causing dyspnea.
[edit] Diagnosis
The diagnosis can be confirmed by the characteristic appearance of the chest x-ray which shows widespread pulmonary infiltrates, and an arterial oxygen level (pO2) strikingly lower than would be expected from symptoms. The diagnosis can be definitively confirmed by pathologic identification of the causative organism in induced sputum or bronchial washings obtained by bronchoscopy with coloration by toluidine blue or immunofluorescence assay, which will show characteristic cysts [2].
Pneumocystis infection can also be diagnosed by immunofluorescent or histochemical staining of the specimen, and more recently by molecular analysis of PCR products comparing DNA samples. Notably, simple molecular detection of Pneumocystis jirovecii in lung fluids does not mean that a person has Pneumocystis pneumonia or infection by HIV. The fungus appears to be present in healthy individuals also in the general population.[12]
Dermatofibrosarcoma protuberans (DFSP) is a rare neoplasm of the dermis layer of the skin, and is classified as a sarcoma. In many respects, the disease behaves as a benign tumor, but in 2-5% of cases it can metastasize, so it should be considered to have malignant potential.
Over 95% of DFSP tumors have the chromosomal translocation t(17;22). The translocation fuses the collagen gene (COL1A1) with the platelet-derived growth factor gene. The fibroblast, the cell of origin of this tumor, expresses the fusion gene in the belief that it is collagen. However the resulting fusion protein is processed into mature platelet-derived growth factor which is a potent growth factor. Fibroblasts contain the receptor for this growth factor. Thus the cell "thinks" it is producing a structural protein, but in fact produces a self-stimulatory growth signal. The cell divides rapidly and a tumor forms.
Treatment is primarily surgical, with chemotherapy and radiation therapy sometimes being used.
There is clinical evidence that imatinib, which inhibits PDGFB, may be effective for tumors positive for the t(17;22) translocation.
