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48 Cards in this Set
- Front
- Back
Describe the pathology?
What is the diagnosis? |
Diagnosis: Acute hepatitis
"Ballooning Degeneration" Description: H/E stain. Hepatocyte injury takes the form of diffuse swelling “ballooning degeneration” so the cytoplasm looks empty and contains only scattered eosinophilic=RED loving :) remnants of cytoplasmic organelles. Note as well the Councillman body. What is that you ask? where should I note it? Great questions! |
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Describe the pathology?
What is the diagnosis? What are the Councilman bodies |
Diagnosis: Acute Viral hepatitis
Description: H/E stain. Hepatocyte injury in the form of diffuse swelling "ballooning degeneration"= note how the cytoplasm looks empty and contains only scattered eosinophilic remnants of cytoplasmic organelles. We already know that.. You want more.. The red bodies are the Councilman apoptotic bodies (hepatocyte apoptosis). They are eosinophilic round bodies containing fragmented nuclei (Red loving as well- sweet/sore because they are dead). Lymphocytes (CD8+ CTLs) and macrophages may also be seen. Woow- wait a min- tell me how does that happen= Pathogenesis: OK, glad to. Basically: the Virus infects the cell --> some viral antigens are presented on the surface of the cell bound to MHC class 1 molecules --> this is recognized by the Cytotoxic CD8+ T cells ( note these are the effector cells- How are these become activated??) So the CD8 binds to MHC 1 on the virus-infected cell --> Cytotoxic CD8+ T cells (CTLs) induce apoptosis of the cell to which they attach: this happens in four stages: 1- attachment: mediated by the T cell receptor, CD8, and LFA-1 integrin 2- activation: inside the CTL, there is cytoskeletal rearrangement to gather and concentrate cytotoxic granules containing preformed proteins 3- Exocytosis of granule content which contains a. Perforin: help to deliver the content into the target cell (Important) by forming a pore in the membrane of the target cell b. Granzyme (important): a serine protease: these pass through the pores to enter the target cell cytoplasm where it activates CASPASES which activate apoptosis. 4- detachment CTLs also kill by two other methods: 1- cytokines: TNF alpha, TNF beta, or Interferon gamma 2- Fas ligand on these cells bind to Fas receptor, thus inducing caspases and in turn apoptosis now, what? Apoptotic hepatocytes shrink, become intensely eosinophilic, and have fragmented nuclei; effector T cells may still be present in the immediate vicinity. Apoptotic cells are rapidly phagocytosed by macrophages and hence might be difficult to find, despite a brisk rate of hepatocyte injury. |
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Describe the pathology?
What is the diagnosis? |
Diagnosis: Hepatitis
Description: Portal and Periportal inflammation. In severe cases of acute hepatitis, confluent necrosis of hepatocytes may lead to bridging necrosis connecting portal-to-portal, central-to-central, or portal-to-central regions of adjacent lobules. Hepatocyte swelling and regeneration compress sinusoids, and the more or less radial array of hepatocyte plates around terminal hepatic veins is lost. The black dots in the picture are lymphocytes. One of the important things in acute hepatitis is lobular disarrangement: which is distortion of the normal liver architecture, loss of sinusoids and may be loss of central veins. This is caused by : 1-Swollen of hepatocytes which compress the sinusoids 2-Some hepatocytes may have more than one nucleus(regeneration),so the architecture become distorted. Inflammation is a characteristic and usually prominent feature of acute hepatitis. Kupffer cells undergo hypertrophy and hyperplasia and are often laden with lipofuscin pigment as a result of phagocytosis of hepatocellular debris. The portal tracts are usually infiltrated with a mixture of inflammatory cells. The inflammatory infiltrate may spill over into the adjacent parenchyma, causing apoptosis of periportal hepatocytes. This is known as interface hepatitis, which can occur in acute and chronic hepatitis. Cells in the canals of Hering proliferate, forming ductular structures at the parenchymal interface (ductular reaction). |
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What are the white and black arrows pointing at?
Describe the pathology? What is the diagnosis? |
Diagnosis: Alcoholic liver disease
Description: H/E stain. Micro-vesicular steatosis. Hepatocytes are larger than usual and contain multiple small cytoplasmic fat droplets that do not displace the nucleus. Need confirmation with red oil O stain. |
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Describe the pathology?
What is the diagnosis? question about steatosis? |
Diagnosis: Alcoholic liver disease
Description: H/E stain. Macro-vesicular steatosis. Hepatocytes are larger than usual and contain a single large cytoplasmic vacuole. In some cells, the nucleus is stretched over the edge of the cell (nucelus is displaced). Note that sections such as the one, are usually made after the tissue has been embedded in paraffin. This process uses several organic solvents which dissolve lipid out of the tissue (vacuole appear empty). Thus to confirm that the vacuoles contain lipid histologically, a different technique, namely a "frozen section" must be performed. In a frozen section, the stain Oil Red O stains lipid thus confirming that the vacuoles in the hepatocytes are lipid rich. |
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Describe the pathology?
What is the diagnosis? |
Diagnosis: Alcoholic liver disease- Mallory Hyaline
Description: Mallory hyaline: Eosinophilic retractile mass containing cytokeratin in the cytoplasm of hepatocytes. |
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What is the pathological diagnosis?
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diagnosis: Centrilobular necrosis due to right heart failure.
Description: Destructed cells around a central vein with nuclear pyknosis, karyorrhexis, karyolysis, and intense cytoplasmic eiosinhophillia. Viable cells are present in the periphery (right side). Toxic causes: 1- Acetaminophen 2- Carbon tetrachloride 3- Mushrooms |
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Identify the tissue type.
What is the pathological diagnosis? |
Tissue: liver
Diagnosis: Piecemeal hepatic necrosis Description : hepatocyte necrosis between periportal parenchyma and inflamed portal tracts. Inflammatory infiltrates (mainly lymphocyte and macrophages). |
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What is the pathological diagnosis?
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Diagnosis: Viral hepatitis- Cholestasis
Description: Hepatocyte dysfunction leading to impaired bile flow. As a result bile pigment accumulates in the hepatocytes, bile canaliculi, and hepatic ducts. Individual hepatocytes are enlarged and have a brownish-green stippled appearance within the cytoplasm, representing bile that cannot get out of the cell. Green-brown plugs of bile can be seen in dilated bile canaliculi or within bile ducts representing bile that has been excreted from the hepatocytes but cannot go any further due to the obstruction. Rupture of canaliculi leads to extravasation of bile, which is quickly phagocytosed by Kupffer cells. Obstruction of the biliary tree, either intrahepatic or extrahepatic, causes distention of upstream bile ducts and ductules by bile. The bile stasis and back-pressure induce proliferation of the duct epithelial cells. The ductules reabsorb secreted bile salts, serving to protect the downstream obstructed bile ducts from their toxic detergent actions. Sufficient pressure (caused by bile accumulation) can cause the ducts to rupture, spilling bile into the surrounding tissue, causing hepatic necrosis( these areas are known as bile lakes, and are typically seen only with extra-hepatic obstruction. |
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What is the pathological diagnosis?
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Diagnosis: Micronodular Alcoholic Cirrhosis
Description: The cut surface of the liver shows micronodular cirrhosis (< 3 mm in diameter) |
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What is the pathological diagnosis?
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Diagnosis: Micronodular Alcoholic Cirrhosis
Description: The cut surface of the liver shows micronodular cirrhosis (<3 mm in diameter). |
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What is the pathological diagnosis?
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Diagnosis: Micronodular Alcoholic Cirrhosis
Description: The cut surface of the liver shows micronodular cirrhosis. Also, the capsular surface shows fibrous thickening. |
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What is the pathological diagnosis?
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Diagnosis: Macronodular Alcoholic Cirrhosis with hepatocellular carcinoma.
Description: The surface of the liver shows macronodular cirrhosis, with the nodules varying in size from a few millimetres to one centimetre and of varying colour. There are also a number of larger, soft partially necrotic masses, up to 5 cms in diameter. These represent foci of malignant change. |
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What is the pathological diagnosis?
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Diagnosis: Macronodular Alcoholic Cirrhosis
Description: Diagnosis: Macronodular Alcoholic Cirrhosis Description: The surface of the liver shows macronodular cirrhosis, with the nodules varying in size from a few millimeters >3 to one centimeter and of varying color. |
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Identify the tissue type.
What is the pathological diagnosis? |
Tissue: liver
Diagnosis: Liver Cirrhosis Description: Masson trichrome stain (stains collagen blue). Normal sinusoidal architecture is rearranged to nodules of regenerating hepatocytes encircled by fibrosis. The diameters of the nodules vary from micronodules (< 3mm) to macronodules (>3mm to several centimeters). The nodularity results from repeated cycles of hepatocytes regeneration and scarring. Bridging fibrous septa in the form of delicate bands or broad scars linking portal tracts with one another and portal tracts with terminal hepatic veins. The parenchymal injury and consequent fibrosis are diffuse, extending throughout the liver disrupting the architecture of the entire liver. Note that: Focal injury with scarring does not constitute cirrhosis, nor does diffuse nodular transformation without fibrosis. |
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What is the pathological diagnosis?
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Diagnosis: Heaptocellular Adenoma
Description: single sucapsular 5 by 3 cm mass well demarcated (+/- encapsulated). It is pale (yellow tan/ bile stained) with varying degrees of hemorrhage and necrosis and homogenous texture. |
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Identify the tissue type.
What is the pathological diagnosis? |
Tissue: liver
Diagnosis: Hepatocellular Adenoma Description: sheets and cords of cells resembling normal hepatocytes (C. Adenoma). Cells and nuclear size are variable. Steatosis is present (white areas indicating fat accumulation). Abundant glycogen may generate large hepatocytes with a clear cytoplasm. There are no portal tracts; instead, prominent solitary arterial vessels and draining veins are distributed through the substance of the tumor (not seen in this view). A- non neoplastic liver: lobules formed by a central vein and peripheral portal tracts B- Fibrous capsule |
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What is the pathological diagnosis?
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Diagnosis: Hepatocellular Carcinoma
Description: Single unifocal large mass replacing the majority of the right lobe in a non-cirrhotic liver. The mass is paler than surrounding tissue. There are areas of yellow-brown areas of hemorrhage, necrosis. Some areas have a green hue: well-differentiated hepatocytes are still viable and capable of secreting bile. |
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Identify the tissue type.
What is the diagnosis? |
Tissue: liver
Diagnosis: Hepatocellular Carcinoma Description: H/E stain. Trabecular pattern. Thick cords separated by sinusoids. Nuclear pleomorphism, vesicular nuclei, chromatin clumping, prominent nucleoli. |
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Identify the organ.
What is the pathological diagnosis. |
Liver Metastases
Description: The cut surface of the liver shows multiple round deposits of tumors that replace hepatic parenchyma. There is a tendency for metastatic nodules to outgrow their blood supply, producing a necrotic haemorrhagic center (umbilication when viewed from the surface of the liver). Always surprising is the amount of metastatic involvement that may be present in the absence of clinical or laboratory evidence of hepatic functional insufficiency. Often the only telltale clinical sign is hepatomegaly, sometimes with nodularity of the free edge. However, with massive destruction of liver substance or direct obstruction of major bile ducts, jaundice and abnormal elevations of liver enzymes may appear. |
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What is the pathological diagnosis?
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Diagnosis: Liver metastases from bronchial carcinoma
What is the route(s) of metastases? |
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What is the pathological diagnosis?
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Diagnosis: Liver metastases from colon carcinoma
What are the route(s) of metastases? |
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What is this organ?
what is the pathological diagnosis? |
Organ: pituitary gland
Diagnosis: Suprasellar Pituitary Adenoma Description: Sellar or Suprasellar mass. The mass may show areas of hemorrhages and/ necrosis. Pathogenesis: The tumor can be functional associated with hypersecretion of hormones (most common types are Prolactinomas, and Growth hormone producing adenoma) or non-functional prouducing hypopituitarism. Prolactinoma: Lab: High prolactin; low LH, FSH, estradiol, and testosterone; Presentation: galactorrhea, amenorrhea, and infertility or decreased libido and impotence. As prolactin provides a negative feedback to Gonadotropin releasing hormone GnRH production by the hypothalamus, which in turn lead to decreased LH and FSH from the anterior pituitary. Growth hormone producing adenom: Lab: high GH, and somoatomedian C= insulin like growth factor 1. Presentation: Gigantism: in children and adolescents prior to fusion of epiphyseal growth plates. Acromegaly in adults after thw grwoth paltes have fused; in addition to MSK enlargment, in acromegaly internal organs are enlarged; commonly the heart leading to cardiac failure (most common cause of death in acromegaly). In addition, GH (counter-regulatory hormone) causes metabolic changes including impaired glucose toelrance and diabetes (opposes actions of insulin). General symptoms/signs typical of pituitary masses include: headaches, visual field deficits: mass compresses the optic chiasma leading to bitemporal hemianopia. |
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Identify the structure indicated by the arrow.
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Superior view of cranial fossa
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What is this organ?
Identify the structure pointed by the arrow? What are some complications that might arise from such a structure? Explain your answer? |
Organ: Thyroid gland
Structure: Thyroglossal Duct Cyst Description: Thyroglossal duct cyst (Arrow). Mucinous, clear secretions collected within the cyst forming a spherical masses or fusiform swellings, (rarely over 2 to 3 cm in diameter). These are present in the midline of the neck anterior to the trachea. Segments of the duct and cysts that occur high in the neck are lined by stratified squamous epithelium, which is essentially identical with that covering the posterior portion of the tongue in the region of the foramen cecum. The anomalies that occur in the lower neck more proximal to the thyroid gland are lined by epithelium resembling the thyroidal acinar epithelium. Characteristically, subjacent to the lining epithelium, there is an intense lymphocytic infiltrate. Pathogenesis: A persistent sinus tract may remain as a vestigial remnant of the tubular development of the thyroid gland. Parts of this tube may be obliterated, leaving small segments to form cysts. These occur at any age and might not become evident until adult life. The cyst is present in the midline of the neck anterior to the trachea The cyst is susceptible to superimposed infection converting these lesions to abscess cavities. Rarely, they give rise to cancer. |
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Identify the tissue type.
What is the diagnosis? |
Tissue: Thyroid
Diagnosis: Papillary carcinoma Description (MICRO):H/E stain. A. Complex branching papillae with fibrovascular stalk (core) covered by single to multple layers of cuboidal epithelial cells. B. Normal thyroid follicles C. Psammoma bodies: Concentrically calcified structures D. The nuclei lining the papillae: dispersed chromatin giving it a clear or empty appearance (1)(ground-glass or Orphan Annie eye nuclei). Also, at high power, invaginations of the cytoplasm into the nucleus give the apperance of intranuclear inclusions (2) (“pseudo-inclusions”) or intranuclear grooves. LOOK VERY CLOSE! The diagnosis of papillary carcinoma is made based on these nuclear features (1-2), even in the absence of papillary architecture. |
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Identify the tissue type.
What is the diagnosis? |
Tissue: Thyroid gland
Diagnosis: Thyroid Medullary Carcinoma Description: Amyloid stain (right half)- immunohistochemistry- immunoperoxidase stain for calcitonin which stains brown (left half). this tumor arises from C cells (parafolicular cells ) and secretes calcitoning. The section sthows nests of polygonal cells in an amyloid stroma. A. Normal thyroid follicles B. Acellular amyloid deposits, derived from altered calcitonin (that is secreted by neoplastic cells) molecules present in the adjacent stoma C. Neoplastic cells are positive for carcitonin. Polygonal to spindle shaped cells in nests, trabeculae, and even follicles. 25% of cases are associated with multiple endocrine neoplasias (MEN) type 2A and 2B. |
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What type of tissue is this?
What is the pathological diagnosis? Identify the labels A-D. What is the underlying pathogenesis? |
Tissue: Thyroid gland-
Diagnosis: Grave’s disease Description: The thyroid gland is usually symmetrically enlarged because of diffuse hypertrophy and hyperplasia of thyroid follicular epithelial cells. Microscopically, the follicular epithelial cells are tall (columnar) and more crowded than usual (C). This crowding results in the formation of small papillae (with no fibrovascular core) (D) which project into the follicular lumen and encroach on the colloid (B). The colloid in the follicular lumen is pale (B) with scalloped margins (A) due to these cells actively resorbing the colloid in the centers of the follicles. Lymphoid infiltrates, consisting predominantly of T cells, with fewer B cells and mature plasma cells, are present throughout the interstitium; germinal centers are common. Pathogenesis: Grave's disease is an autoimmune hyperthyroidism with auto-antibodies (IgG) to thyroid self antigens. The most important autoantibodies are: - thyroid stimulating immunoglobulin: IgG binds to the TSH receptor and mimics the actions of TSH stimulating adenyl cyclase --> increase intracellular cAMP --> activate kinases .... --> 1- release of thyroid hormones 2- enlargment and multiplication of cells. Lab: High T3, T4, Low TSH, detectable thyroid stimulating IgG (very specific for Grave's) - thyroid growth-stimulating immunoglobulins: directed against the TSH receptor -> proliferation of thyroid follicular epithelium. - TSH-binding inhibitor immunoglobulins: These anti–TSH receptor antibodies prevent TSH from binding normally to its receptor on thyroid epithelial cells. These antibodies may sometimes result in stimulation of thyroid function i.e. mimicing TSH or sometimes may inhibit thyroid function (sometimes it happen that Graves disease patients have episodes of hypothyroidism--> this could be the explanation that some antibodies are actually inhibitory!) |
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What is this organ?
Identify the structure pointed by the arrow? What are some complications that might arise from such a structure? Explain your answer? |
Organ: thyroid
Diagnosis: Multinodular Goiter Description: The gland is multolobulated and asymmetrically enlarged with a gelatinous smooth brown (colloid) cut surface. The lobules (A-B) are of uniform size and well demarcated from each other by fibrous tissue septa (C). There are areas of hemorrhage (E) and cystic change (D). There is a lot of colloid there!. Microscopically, see the relevant slide.. The enlarged gland can produce lateral pressure on midline structures, such as the trachea (impede breathing, voice change) and esophagus (difficulty swallowing) . Or the goiter can grow behind the sternum and clavicles (Thoracic inlet syndrome). Pathogenesis: There are focal patches of hyperfunctioning follicular cells working independently of TSH due to mutation in TSH receptor. Thus there is follicular enarlgment and increased colloid formation. There is increased release of T3 and T4 ( HIGH T3, T4, LOW TSH) The morphology of nodular goiters: during goiter growth, some areas may outgrow their blood supply thus leading to hemorrhagic necrosis which result in fibrosis both seen as specific foci of fibrosis and stands of fibrous tissue (C). Thus, the slowly growing number of newly formed follicles (polyclonal: different follicles have different growth rates) has to squeeze into the meshes of an inelastic network of connective tissue. Nodular growth pattern is the inevitable consequence. Some particular nodules expand because of excessive accumulation of colloid. (this is just a thought from an old reference). It is observed though that with diffused goitres, that there is cellular enlargement with very little connective tissue in the interstitial space.. |
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Identify the tissue.
What is the diagnosis? |
Tissue: Thyroid gland
Diagnosis: Multinodular Goiter Description: The follicles are filled with colloid. Their size is variable but non are small. The cells lining the follicles are mostly flattened (inactive) with some areas of hyperplasia. A. colloid filled follicles B. Flattened epithelium C. Fibrous bands D. Areas of follicular epithelial hyperplasia. |
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Identify the tissue type.
What is the diagnosis? |
Tissue: Thyroid gland
Diagnosis: Hashimoto Thyroiditis Description: There are minute aggregations of colloid staining deep red and scattered at wide intervals. Lymphocytic inflammation with germinal centers, replacing normal thryoid folliciles, and epithelial Hurthle cell changes. A. colloid B. Atrophic glands devoid of colloid lined by epithelial cells. C. The epithelial cells are large and clear containing abundant eosionophilic granular cytoplasms= Hurthle cell changes. D. Lymphocytes: infiltrate everywhere forming bands of bluish- staining cells around the lobules and forming germinal centers in some parts. Pathogenesis: Hashimoto's thyroditis is an autoimmune disorder. The inflammation is caused both by CD4+ and CD8+ T-cells as well as plasma cells. CD8+ cytotoxic T-cells are thought to cause direct cell damage via Fas-Fas Ligand interaction leading to apoptosis of thyroid follicular cells whereas CD4+ T-cells release gamma interferon recruiting macrophages that also augment thyroid follicular cell damage. Plasma cells produce antibodies which have specificities against (anti-microsomal and anti-thyroglobulin antibodies) thymoglobulin and thyroid peroxidase resulting in further lack of thyroid hormone production. The Hurthle cell changes are thought to be thyroid follicular cells undergoing metaplastic changes (reversible) as a result chronic inflammation. Cells become large with abundant finely granular eosinophilic cytoplasm and enlarged nuclei. These cells produce very little or none thyroid hormones. However, the hurthle cell changes are not diagnostic alone of Hashimoto's (need to correlate with clinical picture) It is the most common case of chronic hypothyrodism typically presents with painless diffuse enlargment of the thyroid in a middle aged women; however, it may cause a transient HYPERTHYROID picture early in course due to follicular rupture spilling high levels of hormones into the cirulation all at once. There is an increased risk of thyroid lymphoma. |
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What is the diagnosis?
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Organ: Thyroid gland
Diagnosis: Thyroid Adenoma Description: There are two Sphere-shaped well demarcated capsulated tumors in both lobes of the galnd. They have a smooth outline and their cut surface is grayish/white to reddish/brown showing areas of hemorrhage, fibrosis, calcification, or cystification. Pathogenesis: Benign neoplasm derived from follicular epithelium Usually painless, pressure symptoms, usually cold on thyroid scan (if the radio-iodine uptake scan is hot consider toxic adenoma). |
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Identify the organ.
What is the pathological diagnosis? |
Organ: Adrenal glands
Diagnosis: Adrenal Hemorrhage “waterhouse-Frederichsen syndrome” Description: Massive hemorrhage in both adrenals Pathogenesis: caused by overwhelming sepsis commonly due to meningococemia leading to septic shock and disseminated intravascular coagulation induced by lipooligosarraharide endotoxin. |
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Identify the organ.
What is the pathological diagnosis? |
Organ: Adranal gland
Diagnosis: Adrenal Adenoma Description: There is a round tumour about 1-2 cm in diameter. It is well circumscribed with yellowish coloration similar to the color of the cortex. Microscopically, The cells of the tumour reproduce the architecture of the normal glomerulosa layer of the suprarenal cortex. The cells themselves are polygonal and have pinkish foamy cytoplasm. Interstitial tissue is scanty and some of the larger vessels are thrombosed, leading to rather extensive areas of necrosis. The glomerulosa layer produces aldosterone. Hyperaldosteronsim is associated with increased sodium and water reabsorption --> increased plasma volume --> elevation of blood pressure. Also, incerased potassium secretion --> hypokalemia --> heart: arrhytmias, ECG: U and flattened T waves. Muscle: aches, weakness, and paralysis. |
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Identify the organ.
What is the pathological diagnosis? |
Organ: gall bladder
Diagnosis: Acute Cholecystitis and Cholelithiasis Description: A. The serosal surface is remarkably thickned and congested. On the mucosal surface, there is congestion, ulcerations, and inflammatory exudation (pus) B. In addition, gall stones possibly of pigmented or mixed type and green bile are presented in the lumen. |
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Identify the organ.
What is the pathological diagnosis? |
Organ:
Diagnosis: Gall bladder Empyema Description: the gall bladder lumen is distended by a cloudy purulent fluid. The wall is reddish , inflamed and have areas of ulceration , the lumen contain variable sized black stones. |
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Identify the organ.
What is the pathological diagnosis? |
Organ: gall bladder
Diagnosis: Chronic Cholecystitis and Cholelithiasis (cholestrol stones) Description: The wall is thickened and fibrosed but the mucosa is intact. Trabeculations are evident on the luminal side. There are yellowish streaks of cholesterol on the mucosal wall. Cholesterol stones are present. |
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Identify the organ.
What is the pathological diagnosis? |
Organ: gall bladder
Diagnosis: Chronic Cholecystitis and Cholelithiasis (cholesterol stones) Description: Contracted gall bladder. The wall have focal ulcerations and is atrophic. The most striking feature in the cut surfaces of the wall is the presence of numerous large Rokitansky-Aschoff sinuses of varying diameters. These are pseudodivertula or pockets in the wall of the gall bladder. They may be microscopic or macroscopic. Histologically, they are outpouchings of gallbladder mucosa into the gallbladder muscle layer and subserosal tissue. They are not of themselves considered abnormal, but they can be associated with cholecystitis. |
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Identify the organ.
What is the pathology? |
Organ: gall bladder
Pathology: Cholesterolosis Description: small (<= 1mm) yellow mucosal flacks "strawberry Gall bladder". Pathogenesis: Bile supersaturated with cholesterol (no hyperchlesterolemia).. |
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Identify the tissue type. Labels.
What is the diagnosis? |
Tissue: gall bladder
Diagnosis: Cholesterolosis Description: Accumulation of B. cholesterol-laden macrophages within the lamina propria under the surface epithelium (A. simple columnar epithelium).These macrophages are round/polyhedral shaped cells with a centrally located round nucleus with very low nucleus to cytoplasmic ratio (the cytoplasm is filled with cholesterol). C. blood congestion within a vessel |
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Identify the organ.
What is the pathological diagnosis? |
Organ: gall bladder
Diagnosis: Mixed Gall stones Description: The gall bladder is enlarged with thickened walls. The lumen is filled with multiple,tan to grey stones with multifaceted smooth surfaces. |
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Identify the organ?
What is the pathological diagnosis? |
Organ: pancreas
diagnosis: Acute Hemorrhagic pancreatitis Description: The pancreas is enlarged. There are haemorrhagic areas clearly in the body and tail. There are also a few small, chalky-white areas of fat necrosis both in the pancreas and in the fat surrounding it. |
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Identify the organ?
What is the pathological diagnosis? What is the underlying pathogenesis? |
Organ: pancreas
Diagnosis: Acute Hemorrhagic pancreatitis Description: The top half of the picture is the serosal surface of a normal duodenum with its associated fat covered mesentery. The lower half of the picture is a hemorrhagic enlarged pancreas (black). Gross characteristics of acute pancreatitis are proteolysis and lipolysis of the pancreas and the surrounding tissue which are seen as hemorrhage and fat necrosis, respectively. Pathogenesis: The pathogenesis of acute pancreatitis is not fully understood but most cases appear to occur in patients with gall stones or in alcoholics. Reflux of bile into the pancreatic ducts may be an important triggering event. It is thought that activation of destructive Pancreatic enzymes is important in leading to the PANCREATIC NECROSIS and also HAEMORRHAGE which follows enzymatic destruction of vessel walls. The fat necrosis is thought to be due to the action of LIPASES released from the pancreas. These convert the TRIGLYCERIDES in the fat depots to FATTY ACIDS which may then CALCIFY. GLYCEROL is also formed but this probably diffuses away from the area. In patients with suspected acute pancreatitis, it is usually considered helpful to measure the serum amylase. This enzyme is also released into the blood from necrotic pancreatic tissue but elevation of serum amylase occurs in conditions other than acute pancreatitis (NON-SPECIFIC). |
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Identify the organ?
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Organ: normal pancreas second part of the duodenum
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Identify the organ?
What is the pathological diagnosis? Describe the pathology? What do you expect to find on microscopic and radiological examination? |
Organ: pancreas
Diagnosis: Chronic pancreatitis Description: There is diffuse atrophy (shrunken) and fibrosis (hard). The main pancreatic duct is dilated and filled with calcified concretions (protein plugs). Pseudocysts are commonly found (As necrotic pancreatic tissue liquefies, it forms a "pseudo cyst".This may be in the region of the pancreas or extend beyond the pancreatic region). The cut surface of the pancreas and the fat surrounding it, may contain chalky white nodules up to 0.5 cm in diameter which represent fat necrosis. Microscopically: extensive fibrosis, parenchymal atrophy, and chronic inflammation. Fat necrosis is seen, with each area having undergone calcification. Radiology (erect film of the abdomen), extensive calcification can be seen scattered obliquely from L2 and L3 on the right, upwards to the left of L1. This indicates chronic pancreatitis. |
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Identify the organ?
Describe the pathology in this specimen? What is your diagnosis? |
Organ: Cross section of the pancreas
Description: extensive fibrosis. Dilated main pancreatic duct filled with calcified secretions. Diagnosis: Chronic pancreatitis |
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Identify the organ?
What is the pathological diagnosis? Describe the pathology? What signs and symptoms do you expect in this patient? |
Organ: Pancreas
Diagnosis: Cancer of the head of pancreas Description: the head of the pancreas is replaced by a hard (solid) pale tumor. The infiltrative margins are poorly defined and there are areas of necrosis. The body and tail are generally normal. Microscopically, the adenocarcinoma arises from the duct epithelium. Extensive areas of chronic inflammation are expected. Presentation: usually presents with non specific symptoms until late in the disease course. More definitive symptoms include abdominal pain, migratory thrombophlebitis, and obstructive jaundice. Obstructive jaundice: In this case, as the mass is infiltrating the head where the common bile duct (CBD) pass through to join the main pancreatic duct, thus obstructing bile flow into the duodenum. It presents with yellow discoloration of the mucosal tissue in the skin, and sclera. Lab results: high total bilirubin, high conjugated bilirubin, elevated Serum alkaline phosphatase, 5 nucelosidase, and GGT. Moreover, the tumour markers for pancreatic carcinoma include CEA and CA19-9. Migratory thrombophlebitis: this is called "Trousseau Syndrome": spontaneous venous thrombosis that start in one area and then may resolve and recur in other areas. It is commonly associated with visceral malignancy due to the release of mucin from the tumor. The mucin initiates the extrinsic pathway of coagulation. |
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Indicates chronic pancreatitis
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Not assessed.
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