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	<title>Pathology Biology and Diseases</title>
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	<link>http://www.biologydisease.com</link>
	<description>Information on Pathology, Biology, Animals, Plants, Microbes and Diseases. BiologyDisease.com © 2012</description>
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		<title>Alzheimer&#8217;s Disease Pathology</title>
		<link>http://www.biologydisease.com/brain/alzheimer-disease/</link>
		<comments>http://www.biologydisease.com/brain/alzheimer-disease/#comments</comments>
		<pubDate>Thu, 25 Aug 2011 00:44:11 +0000</pubDate>
		<dc:creator>admin</dc:creator>
				<category><![CDATA[Brain]]></category>
		<category><![CDATA[Alzheimer's Disease]]></category>
		<category><![CDATA[Amyloid angiopathy]]></category>
		<category><![CDATA[diffuse plaques]]></category>
		<category><![CDATA[Hirano bodies]]></category>
		<category><![CDATA[Neurofibrillary Tangles]]></category>
		<category><![CDATA[senile neuritic plaques]]></category>

		<guid isPermaLink="false">http://www.biologydisease.com/?p=1910</guid>
		<description><![CDATA[Alzheimer&#8217;s Disease Pathology Alzheimer&#8217;s disease gross and light microscopic features Gross &#8211; variable degree of cortical atrophy with widening of the cerebral sulci that is msot pronoucned in the frontal, temporal, and parietal lobes - with significant atrophy, there is compensatory ventricular enlargement secondary to loss of parenchyma &#160; LM &#8211; neurofibrillary tangles, senile (neuritic) plaques, amyloid angiopathy - neurofibrillary tangles:  bundles of filaments in the cytoplasm fo the neurons that displace or encircle the nucleus - often have an elongated “flame” shape - in some cells, the basket weave of fibers around the nucleus takes on a rounded contour (globose tangles) - visible as basophilic fibrillary structures with H&#38;E staining but dramatically demonstrated by silver (Bielschowsky) staining - commonly found in cortical neurons, especially in the entorhinal cortex, as well as in otehr sites such as pyramidal cells of the hippocampus, the amygdala, the basal forebrain, and the raphe nuclei - tangles insoluble and apparently difficutl to proteolyzxe in vivo, thus remaining visible in tissue sections as “ghost” or “tombstone” tangles long after the death of the parent neuron - stain with tau, ubiquitin, amyloid b-peptide (Ab) - neuritic plaques:  focal, spherical collections of dilated, tortuous, silver-staining neuritic processes (dystrophic neurites) surrounding a central amyloid core, often surrounded by clear halo - range in size from 20-200 mm in diameter - microglial cells and reactive astrocytes present at their periphery - found in hippocampus and amygdala as well as in neocortex - usually relative sparing of primary motor and sensory cortices (this also applies for neurofibrillary tangles) - amyloid core can be stained by Congo red and Bielschowsky silver methods - amyloid core contains several abnormal proteins, stains with Ab - Ab immunostaining demonstrates existence, in some patients fo amyloid peptide deposits of lesions lacking the surrounding neuritic reaction - these lesions called diffuse plaques, found in superficial portison fo cerebral cortex as well as in basal ganglia and cerebellear cortex - commonly when diffuse plaques found in cerebral cortex, they appear to be centered on small vessels or on clusters of neurons - diffuse plaques may represent early stage of neuritic plaque development - amyloid angiopathy almost always present - vascular amyloid derived from same precursor as amyloid cores of plaques (APP) - granulovacuolar degeneration:  formation of small (5 mm) clear intraneuronal cytoplasmic vacuoles, each of which contains an argyrophilic granule - found in great abundance in hippocampus and olfactory bulb in Alzheimer’s - Hirano bodies:  elongated glassy eosinophilic bodies consisting of paracrystalline arrays of beaded filaments, with actin as major component - found most commonly along hippocampal pyramidal cells &#160; Alzheimer&#8217;s disease clinical features initially &#8211; forgetfulness and other memory disturbances - insidious impairment of higher intellectual function - alterations in mood and behaviour with progression &#8211; language deficits (aphasia) - disorientation - loss of mathematical skills - loss of learned motor skills final stages &#8211; incontinence - muteness - inability to walk common terminal event &#8211; pneumonia &#160; Alzheimer&#8217;s disease pathogenesis - see above &#160; Alzheimer&#8217;s disease gross features of the brain - cortical atrophy - widening of cerebral sulci (most severe in frontal, temporal, parietal lobes) - ventricular enlargement &#160; Alzheimer&#8217;s disease microscopic features of the brain - neurofibrillary tangles - senile (neuritic) plaques - amyloid angiopathy - diffuse plaques - granulovacuolar degeneration - Hirano bodies Diagnostic criteria - neurofibrillary tangles, senile (neuritic) plaques, amyloid angiopathy can all be seen to a lesser extent in brains fo elderly nondemented individuals - diagnosis of Alzheimer disease based on a combination of clinical and pathologic features - several different methods proposed, which include evaluation of different regions of the brain and various methods for estimating the frequency of plaques and tangles References: 1. Robbins &#38; Cotran Pathologic Basis of Disease, 8th edition. Vinay Kumar, MBBS, MD, FRCPath; Abul K. Abbas, MBBS; Nelson Fausto, MD; Jon Aster, MD. Saunders. Published June 2009. 2. Sternberg’s Diagnostic Surgical Pathology, 5th edition. Darryl Carter, Joel K. Greenson, Victor E. Reuter , Mark H. Stoler. Lippincott Williams &#38; Wilkins. Published Aug 26 2009.]]></description>
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		<item>
		<title>Amyloidosis</title>
		<link>http://www.biologydisease.com/anatomic-pathology/amyloidosis-diseases/</link>
		<comments>http://www.biologydisease.com/anatomic-pathology/amyloidosis-diseases/#comments</comments>
		<pubDate>Thu, 25 Aug 2011 00:37:14 +0000</pubDate>
		<dc:creator>admin</dc:creator>
				<category><![CDATA[Anatomic Pathology]]></category>
		<category><![CDATA[Alzheimer disease]]></category>
		<category><![CDATA[amyloid]]></category>
		<category><![CDATA[Amyloidosis]]></category>
		<category><![CDATA[Atrial natriuretic fact]]></category>
		<category><![CDATA[ATTR]]></category>
		<category><![CDATA[beta2 -microglobulin]]></category>
		<category><![CDATA[CLASSIFICATION OF AMYLOIDOSIS]]></category>
		<category><![CDATA[Familial amyloidotic neuropathies]]></category>
		<category><![CDATA[Familial Mediterranean fever]]></category>
		<category><![CDATA[Generalized Amyloidosis]]></category>
		<category><![CDATA[Hemodialysis-associated amyloidosis]]></category>
		<category><![CDATA[Hereditary amyloidosis]]></category>
		<category><![CDATA[Islet of Langerhans]]></category>
		<category><![CDATA[Isolated atrial amyloidosis]]></category>
		<category><![CDATA[Localized Amyloidosis]]></category>
		<category><![CDATA[Medullary carcinoma of thyroid]]></category>
		<category><![CDATA[primary amyloidosis]]></category>
		<category><![CDATA[secondary amyloidosis]]></category>
		<category><![CDATA[Senile cerebral]]></category>
		<category><![CDATA[Systemic Amyloidosis]]></category>
		<category><![CDATA[Systemic senile amyloidosis]]></category>
		<category><![CDATA[Transthyretin]]></category>
		<category><![CDATA[Ultrastructural features of amyloid]]></category>

		<guid isPermaLink="false">http://www.biologydisease.com/?p=1907</guid>
		<description><![CDATA[Amyloidosis CLASSIFICATION OF AMYLOIDOSIS Clinicopathologic Category Associated Diseases Major Fibril Protein Chemically Related Precursor Protein Systemic (Generalized) Amyloidosis Immunocyte dyscrasias with amyloidosis (primary amyloidosis) Multiple myeloma and other monoclonal B-cell proliferations AL Immunoglobulin light chains, chiefly lambda type Reactive systemic amyloidosis (secondary amyloidosis) Chronic inflammatory conditions AA SAA Hemodialysis-associated amyloidosis Chronic renal failure Abeta2 m beta2 -microglobulin Hereditary amyloidosis Familial Mediterranean fever &#8211; AA SAA Familial amyloidotic neuropathies (several types) &#8211; ATTR Transthyretin Systemic senile amyloidosis &#8211; ATTR Transthyretin Localized Amyloidosis Senile cerebral Alzheimer disease Abeta APP Endocrine Medullary carcinoma of thyroid &#8211; A Cal Calcitonin Islet of Langerhans Type II diabetes AIAPP Islet amyloid peptide Isolated atrial amyloidosis &#8211; AANF Atrial natriuretic fact &#160; AL  amyloid light chain AA amyloid-associated TTR Transthyretin APP amyloid precursor protien &#160; Ultrastructural features of amyloid By electron microscopy, amyloid is seen to be made up largely of non branching fibrils of indefinite length and a diameter of approximately 7.5 to 10 nm. This electron microscopic structure is identical in all types of amyloidosis. X-ray crystallography and infrared spectroscopy demonstrate a characteristic cross beta-pleated sheet conformation. This conformation is seen regardless of the clinical setting or chemical composition and is responsible for the distinctive staining and birefringence of Congo red-stained amyloid. In addition to amyloid fibrils, other minor components are always present in amyloid. These include serum amyloid P component, proteoglycans, and highly sulfated glycosaminoglycans. These nonproteinaceous substances are presumably derived from the connective tissue in which amyloid is deposited. &#160; Histochemical stains for Amyloidosis 1 &#8211; As noted earlier, the histologic diagnosis of amyloid is based almost entirely on its staining characteristics. The most commonly used staining technique employs the dye Congo red, which under ordinary light imparts a pink or red color to amyloid deposits. Under polarized light, the Congo red- stained amyloid shows a green birefringence. This reaction is shared by all forms of amyloid and is due to the cross-beta-pleated configuration of amyloid fibrils. Confirmation can be obtained by electron microscopy. 2 – Potassium permanganate pretreatment of sections , has been used to distinguish amyloid type AA (sensitive to effect of pretreatment) from non-type AA amyloids (resistant) .The underlying mechanism is unknown .Recently , however , the specificity of potassium permanganate for this differentiation has been called into question. Both thioflavin T and S have been used for the demonstration of amyloid. Although these dyes have high levels of sensitivity , their specificity is less than that of Congo Red. References: 1. Robbins &#38; Cotran Pathologic Basis of Disease, 8th edition. Vinay Kumar, MBBS, MD, FRCPath; Abul K. Abbas, MBBS; Nelson Fausto, MD; Jon Aster, MD. Saunders. Published June 2009. 2. Sternberg’s Diagnostic Surgical Pathology, 5th edition. Darryl Carter, Joel K. Greenson, Victor E. Reuter , Mark H. Stoler. Lippincott Williams &#38; Wilkins. Published Aug 26 2009.]]></description>
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		<item>
		<title>Acute Tubular Necrosis</title>
		<link>http://www.biologydisease.com/kidney/acute-renal-failure-acute-tubular-necrosis/</link>
		<comments>http://www.biologydisease.com/kidney/acute-renal-failure-acute-tubular-necrosis/#comments</comments>
		<pubDate>Thu, 25 Aug 2011 00:25:34 +0000</pubDate>
		<dc:creator>admin</dc:creator>
				<category><![CDATA[Kidney]]></category>
		<category><![CDATA[Acute renal failure]]></category>
		<category><![CDATA[Acute Tubular Necrosis]]></category>
		<category><![CDATA[atn]]></category>
		<category><![CDATA[disturbances in blood flow]]></category>
		<category><![CDATA[Ischemic Acute Tubular Necrosis]]></category>
		<category><![CDATA[NEPHROTOXIC acute tubular necrosis]]></category>
		<category><![CDATA[tubular cell injury]]></category>

		<guid isPermaLink="false">http://www.biologydisease.com/?p=1904</guid>
		<description><![CDATA[ACUTE TUBULAR NECROSIS (ATN) What is acute renal failure? -an abrupt decline in renal function over hours to days -failure of the kidney to excrete waste products leading to a rise in serum urea and creatinine, usually with decreased urine output (&#60;400ml/24h) -variable other physical and biochemical abnormalities depending on duration of renal insufficiency (esp. electrolytes) -traditionally divided into 3 etiologies: prerenal renal post renal -prerenal and ATN can be viewed as part of a continuum and are the most common causes of ARF in a hospitalized patient. ATN=reversible destruction of tubular epithelial cells associated with acute suppression of renal function Microscopic features of ISCHEMIC acute tubular necrosis -patchy, focal tubular epithelial necrosis, with rupture of tubular basement membranes (tubulorrhexis) and luminal occlusion by casts -PCT and ascending thick limb most susceptible, but focal necrosis with casts can be seen in distal tubules -epithelial cells show a spectrum of changes depending on severity and evolution of lesion: -cell swelling, dilatation of proximal tubules, and varying degrees of necrosis and sloughing of epithelium -eosinophilic hyaline and granular casts seen predominantly in distal tubule and collecting ducts -consist of Tamm-Horsfall protein (urinary glycoprotein usually secreted by these cells) with Hb, myoglobin, other proteins and cell debris -with time see evidence of regeneration * -flattened epithelial cells -hyperchromatic, large nuclei -mitotic activity -interstitial edema and WBC in vasa recta (vascular supply) Microscopic features of NEPHROTOXIC acute tubular necrosis -extensive epithelial necrosis predominantly affecting the proximal tubules (classically NOT patchy) -also see eosinophilic and granular casts in distal tubules and collecting ducts -“classic” changes associated with different etiologic agents: -ethylene glycol: ballooning and vacuolar degeneration of PCT with deposition of oxalate crystals in tubular lumina -lead: dark intranuclear inclusions -CCl4: lipid accumulation -hemoglobin/myoglobin: multiple deeply pigmented dark red/brown casts -tubulitis is NOT a feature of ATN Acute Tubular Necrosis Critical Events a)tubular cell injury b)disturbances in blood flow -tubule cells sensitive to ischemia →structural (reversible and irreversible) and biochemical (ie. activation of proteases and phospholipases) abnormalities -loss of cell polarity with redistribution of membrane proteins →abnormal ion transport across cells and increased Na to distal tubules →tubuloglomerular feedback and vasoconstriction -expression of cytokines and adhesion molecules, accumulation of inflam cells -sloughed, injured cells are incorporated in casts causing luminal obstruction -ischemic injury incites hemodynamic changes causing decreased GFR -intrarenal vasoconstriction through various mechanisms: -direct ischemic injury to glomeruli -renin/angiotensin activation stimulated by tubuloglomerular feedback -direct endothelial cell injury with release of vasoconstrictor mediators -regeneration of tubular epithelial cells possible when and if inciting agent is removed -dependent on cytokines and growth factors produced by both the tubular cells themselves and inflammatory cells in the vicinity ie. EDGF, TGFα, IGF, HepGF]]></description>
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		</item>
		<item>
		<title>Cervical Cancer Staging</title>
		<link>http://www.biologydisease.com/cervix/cervical-cancer-staging/</link>
		<comments>http://www.biologydisease.com/cervix/cervical-cancer-staging/#comments</comments>
		<pubDate>Sun, 31 Jul 2011 01:53:31 +0000</pubDate>
		<dc:creator>admin</dc:creator>
				<category><![CDATA[Cervix]]></category>
		<category><![CDATA[Cancer staging]]></category>
		<category><![CDATA[Cervical Cancer Staging]]></category>
		<category><![CDATA[Cervical cancer synoptic report]]></category>
		<category><![CDATA[Cervix Grossing]]></category>
		<category><![CDATA[Grossing]]></category>
		<category><![CDATA[Specimen grossing]]></category>
		<category><![CDATA[Staging]]></category>
		<category><![CDATA[Surgical pathology grossing]]></category>
		<category><![CDATA[Synoptic report]]></category>

		<guid isPermaLink="false">http://www.biologydisease.com/?p=1535</guid>
		<description><![CDATA[Cervical Cancer Staging Tx &#8211; cannot be assessed T0 &#8211; no evidence of primary tumor T1a &#8211; microscopically invasive T1a1 &#8211; &#60;3mm deep, 7mm wide T1a2 &#8211; &#60;5mm deep, 7mm wide T1b &#8211; visible invasion T1b1 &#8211; &#60;4cm T1b2 &#8211; &#62;4cm T2 &#8211; beyond uterus T3 &#8211; pelvic wall OR lower 1/3 vagina T4 &#8211; bladder/rectum Measuring depth of invasion Cervix Grossing CONE BIOPSY 1. open at 12 o’clock (open like this:“O”?”U”) 2. pin on corkboard with mucosa up and fix 3. ink margins 4. cut parallel sections and submit from 12-3, 3-6,6-9 and 9-12 o’clock &#38; mark on drawing 5. submit in toto SYNOPTIC REPORT CONE BIOPSY Macroscopic tumor site (quadrant: either 12-3, 3-6, 6-9 or 9-12 o’clock) Tumor size Histologic tumor type (WHO) Tumor grade Depth of invasion (mm) Width (horizontal extent) of tumor (mm) Margins (endocervical, exocervical, deep) margin &#8211; involved by intraepithelial/invasive carcinoma (focal or diffuse) or __ mm from closest invasive carcinoma HYSTERECTOMY Specimen type Other organs present Macroscopic tumor site (quadrant: either 12-3, 3-6, 6-9 or 9-12 o’clock) Tumor size Histologic tumor type (WHO) Tumor grade Depth of invasion (mm) pTNM / FIGO staging Margins Distal margin &#8211; involved or not involved by carcinoma in situ]]></description>
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		</item>
		<item>
		<title>Pediatric Renal Tumors</title>
		<link>http://www.biologydisease.com/kidney/pediatric-renal-tumors/</link>
		<comments>http://www.biologydisease.com/kidney/pediatric-renal-tumors/#comments</comments>
		<pubDate>Mon, 25 Jul 2011 01:18:44 +0000</pubDate>
		<dc:creator>admin</dc:creator>
				<category><![CDATA[Kidney]]></category>
		<category><![CDATA[Pediatric Cancers]]></category>
		<category><![CDATA[Pediatric Renal Tumors]]></category>
		<category><![CDATA[Pediatric Tumors]]></category>
		<category><![CDATA[Renal Tumors]]></category>

		<guid isPermaLink="false">http://www.biologydisease.com/?p=1695</guid>
		<description><![CDATA[Pediatric Renal Tumors Nephrogenic Rests Wilm&#8217;s Tumor (Nephroblastoma) Metanephric Adenoma Mesoblastic Nephroma Clear Cell Sarcoma Rhabdoid Tumor Ossifying Renal Tumor of Infants]]></description>
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