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Tag Archives: carcinoma
Crohns Disease
Crohn’s Disease
Epidemiology:
- associated with HLA DR1/DQw5, white, smokers
Location: throughout GI tract, most common in small bowel and also in colon with rectal sparing
Symptoms: episodic mild diarrhea, pain, blood in stool, mucous in stool
Extraintestinal symptoms:
Arthritis (migratory polyarthritis)
Sacroilitis
Ankylosing spondylitis
Progressive sclerosing cholangitis
Erythema Nodosum
Complications: fibrosing strictures; fistulas to bowel, bladder, vagina and perianal skin; protein losing enteropathy, malabsorption, Vitamin B12 deficiency, bile salt malabsorption with steatorrhea, carcinoma
Treatment: steroids, surgery eventually
Gross appearance:
mucosa: aphthous and linear ulcers, skip lesions (sharp demarcation), cobblestone
wall: edema, thickening, fibrosis,
serosa: sinus tracts, fistulae, creeping fat
Histology:
- superficial or deep ulcers, neutrophils within crypt abscesses
- Paneth cell and pyloric gland metaplasia
- features of chronicity
wall and serosa:
- non-necrotizing granulomatous inflammation – may need serial sections to find
- transmural inflammation with lymphoid aggregates
- fibrosis of submucosa, muscularis propria; hyperplasia of muscularis propria
- serositis
Dysplasia and carcinoma:
Poor prognosis: long duration and severe disease
Posted in Colon
Tagged Ankylosing spondylitis, Arthritis, bile salt malabsorption with steatorrhea, Blood in stool, Bloody stool, carcinoma, Colon discomfort, Colon pain, Colonic pain, Crohn disease, crohns disease, Crohns disease findings, erythema nodosum, Extraintestinal symptoms, IBD, Inflammation of the colon, Inflammatory Bowel Disease, Malabsorption, migratory polyarthritis, Progressive sclerosing cholangitis, protein losing enteropathy, Sacroilitis, Vitamin B12 deficiency
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Carcinoma of Unknown Primary
Cancer Type Carcinoma of Unknown Primary
Carcinoma of Unknown Primary Information on Symptoms, Diagnosis, Prognosis, Screening and Imaging
Cancer of Unknown Primary Site Cancers of unknown primary sites present as metastatic cancers for which precise primary tumor sites cannot be determined. As an example, lymph nodes at the base of the skull may enlarge in relationship to a tumor that may be on the face or the scalp but not evident by physical examination or by x-ray. Thus, the extent of the disease may be evident, but a primary site is not evident. For all patients who present with tumors of unknown primary sites, treatment should be considered in relation to the pathology of the tumor, and treatment appropriate for the general type of cancer should be initiated, regardless of the site or sites of involvement. Depending on histologic findings, symptoms, and the extent of tumor, appropriate and relevant chemotherapy and radiation therapy treatments should be initiated as early as feasible.
Posted in Cancer
Tagged Cancer, carcinoma, carcinoma of unknown primary information, diagnosis, imaging, information, prognosis, screening, symptoms
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Yolk Sac Tumour
Yolk Sac Tumour
Clinical Information
- most common testicular tumor are in kids <3 and young adults, serum AFP most important
Gross Appearance
- yellow-gray nodule, often with hemorrhage and necrosis
Microscopic Appearance
Variants of yolk sac tumours
- endodermal sinus pattern (Schiller-Duval bodies)
-microcystic (reticular)
-others: hepatoid, solid, glandular
-hyaline globules (DPAS, AFP, AAT+) (outside cells)
Yolk Sac Immunohistochemistry
-diffuse AFP alpha feto protein, cytokeratin CK
Cancer Calcifications
Cancer Calcifications
Posted in Breast, Cancer, Prostate
Tagged , Breast, calcification, calcifications, Cancer, carcinoma, detection, Prostate
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Adenoid Cystic Carcinoma
Adenoid Cystic Carcinoma
Gross
Small, poorly encapsulated, infiltrative, gray-pink
Histology
a. Basaloid tumour, consisting of epithelial and myoepithelial cells
b. Growth patterns – tubular, cribiform, solid
c. Microcystic and pseudoglandular spaces filled with hyaline or basophilic mucoid material
d. Perineural invasion is common
Clinical
a. Slow growing mass, most frequently involving parotid, submandibular, minor salivary glands
b. Pain with perineural invasion
c. High rate of recurrence
d. 50% disseminate widely, sometimes decades after resection
Poor prognostic factors:
Minor salivary gland
Larger size
Facial nerve paralysis
Histologic pattern (solid)
Recurrence
Metastasis
Differential Diagnosis:
Basal cell adenoma/adenocarcinoma
Polymorphous low-grade adenoca
Pleomorphic adenoma
Treatment:
- radiosensitive; resection
Posted in Salivary Gland
Tagged , adenoid cystic, Adenoid cystic carcinoma, Breast, carcinoma, Salivary Gland, tumor
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Myoepithelioma
Myoepithelioma
Posted in Salivary Gland
Tagged , carcinoma, myoepithelial, Myoepithelioma, Salivary Gland, tumor
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Pleomorphic Adenoma
Pleomorphic Adenoma
Pleomorphic Adenoma Gross Features
Round, well-demarcated, encapsulated (not always well-developed)
Expansile growth with tonguelike protrusions
Cut surface is gray-white with myxoid and blue translucent areas
- Well-defined ovoid tumours, encapsulated (except in minor glands)
Bossellated outer surface
- Cut surface is homogeneous, white or tan; glistening appearance where there are cartilaginous or myxochondroid areas
Microscopic Features
Mixture of epithelial and myoepithelial cells
Myoepithelial cells are arranged in various patterns (tubules, strands, sheets…) and are dispersed within a loose myxoid background
May see islands of chondroid or bone
May see squamous metaplasia
Clinical:
Painless, slow-growing, mobile, discrete mass
Location: parotid, submandibular or buccal cavity
Incidence of malignant transformation increases with duration of tumour (2% for less than 5 yrs; 10% for more than 15 yrs)
Treatment:
Recurrence rate of 4% with adequate parotidectomy; 25% with enucleation
Posted in Salivary Gland
Tagged , carcinoma, PA, Pleomorphic adenoma, Salivary Gland, tumor
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Familial Adenomatous Polyposis Syndrome
Familial Adenomatous Polyposis (FAP) Syndrome
Familial Adenomatous Polyposis Syndrome Inheritance pattern
- autosomal dominant inheritance
- APC gene is on chromosome 5q21
- APC gene plays a role in the WNT pathway in the degradation of the beta-catenin
- beta-catenin role is to turn on transcription factors in the nucleus that lead to cell cycle progression
-mutations in the APC leads to absence of b-catenin degradation and signal independent tranlocation into the nucleus where it turns on the cell cycl
Familial Adenomatous Polyposis Syndrome Clinical Presentation
- two types of clinical presentations:
Classic Familial Adenomatous Polyposis
- minimum of 100 colonic polyps
- polyps in ampulla of Vater – this leads to a prophylactic colectomy in siblings and first-degree relatives which are at risk
Attenuated Familial Adenomatous Polyposis
- patients tend to develop fewer polyps (average 30), and most of the polyps are located in the proximal colon
- lifetime risk of cancer development is usually around 50%
Gardner syndrome
- polyps identical to those in classic FAP
- multiple osteomas (particularly of the mandible, skull, and long bones)
- epidermal cysts
- fibromatosis – desmoid tumors
- less frequent are abnormalities of dentition, such as unerupted and supernumerary teeth
- higher frequency of duodenal and thyroid cancer
Turcot syndrome
- combination of adenomatous colonic polyposis and tumors of the CNS
2/3 have have APC gene mutations and develop brain medulloblastomas
- 1/3 have mutations in one of the genes associated with HNPCC and develop brain glioblastomas
Gross Features of Familial Adenomatous Polyposis
-hundreds to thousands of adenomas evenly distributed through colorectum and appendix
- adenomas range from microscopic to 1cm in diameter with larger adenomas found in the rectosigmoid
- rectum occasionally spared, especially in the attenuated FAP
- colorectal carcinomas may be multifocal
Microscopic Features of Familial Adenomatous Polyposis
- histologically identical to sporadic adenomas
- normal intervening mucosa
- adenomas evolve from single adenomatous crypts
Symptoms and Management
- patients may be asymptomatic before puberty
- initial symptoms are rectal bleeding and diarrhea
- carcinomas start about 6 years after first symptoms
- 100% colon cancer without intervention
- treatment is prophylactic total colectomy
- following colectomy, the most common cause of death is periampullary cancer in 20%
Posted in Colon, GI, Syndrome
Tagged , adenoma, apc, apc gene, b-catenin, Cancer, carcinoma, Colon, colorectal, Familial Adenomatous Polyposis, gardner, periampullary cancer, polyps, Syndrome, turcot
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Small Cell Lung Cancer
Small Cell Lung Cancer
Clinical Information
- 25% of all lung cancers are small cell lung cancers
- there is a very strong association with smoking
- paraneoplastic syndrome common such as inappropriate anti-diruetic hormone secretion and Cushing s due to excess steroid secretion
- present as central tumors, hilar and peri-hilar
- metastasizes very early on
- extensive lymph node metastases are commonly seen
- treated with chemotherapy (very responsive but recurs often)
- radiation therapy only if localized
Small cell lung cancer appears microscopically as:
- round to fusiform nuclei with strong nuclear molding
- nucleoli are faint or absent
- very little to scant cytoplasm
- extensive necrosis common
- basically three histologic patterns:
- Small cell pattern only
- Mixed small cell and large cell pattern
- Mixed with other lung cancer patterns such as squamous, adenocarcinoma
Differential Diagnosis
- non-small cell carcinoma, such as large cell lung cancer
but these other tumors have:
- larger nuclei
- prominent nucleoli
- lack nuclear molding and have a lower nuclear/cytoplasmic ratio
Image (above) of small cell lung cancer, showing typical nuclear features, abundant mitoses and pleomorphism.
Small Cell Lung Cancer Immunohistochemistry
Small cell lung cancer is positive for:
- neuroendochrine markers: chromogranin, synaptophysin, CD56
- thyroid transcription factor 1 TTF-1
- Leu-7
- HOWEVER – around a quarter are not positive for any neuroendocrine markers
Image (below) of synaptophysin immunohistochemistry in small cell lung cancer.
Image (below) of thyroid transcription factor 1, TTF-1, immunohistochemistry in small cell lung cancer, demonstrating that the tumor is of lung origin.
Molecular Biology and Genetics of Small Cell Lung Cancer
- 3p deletions most common, but there are many other genetic alterations