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	<title>PG Blazer &#187; Pathology</title>
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		<title>AFMC 2011 &#8211; MCQ 26</title>
		<link>http://pgblazer.com/2011/01/afmc-2011-mcq-26.html</link>
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		<pubDate>Wed, 19 Jan 2011 23:58:24 +0000</pubDate>
		<dc:creator>pgblazer</dc:creator>
				<category><![CDATA[AFMC 2011]]></category>
		<category><![CDATA[Pathology]]></category>

		<guid isPermaLink="false">http://pgblazer.com/?p=3945</guid>
		<description><![CDATA[Auer rods are seen in?
A. AML
B. CML
C. CLL
D. ALL
   
 
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			<content:encoded><![CDATA[<p>Auer rods are seen in?<br />
A. AML<br />
B. CML<br />
C. CLL<br />
D. ALL</p>
<div class="plus-one-wrap"><g:plusone size="medium" href="http://pgblazer.com/2011/01/afmc-2011-mcq-26.html"></g:plusone></div>   
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		<title>Burtonian line (Lead line)</title>
		<link>http://pgblazer.com/2011/01/burtonian-line-lead-line.html</link>
		<comments>http://pgblazer.com/2011/01/burtonian-line-lead-line.html#comments</comments>
		<pubDate>Thu, 06 Jan 2011 00:16:30 +0000</pubDate>
		<dc:creator>pgblazer</dc:creator>
				<category><![CDATA[Forensic medicine]]></category>
		<category><![CDATA[Pathology]]></category>

		<guid isPermaLink="false">http://pgblazer.com/?p=3736</guid>
		<description><![CDATA[
Burtonian line, also known as lead line is a clinical manifestation of chronic lead poisoning
It is a stippled blue line seen in 50-70% of patients with chronic lead poisoning
It is manifested as a bluish black line due to epidermal deposition of lead sulphate at the junction of the gums with the teeth (not seen on the teeth)
Similar pigmented lines are seen in poisoning with mercury, copper, silver, bismuth and iron poisoning
Other features of chronic lead poisoning include pallor (anemia), constipation, paralysis and lead encephalopathy

   
 
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			<content:encoded><![CDATA[<ul>
<li>Burtonian line, also known as lead line is a clinical manifestation of chronic lead poisoning</li>
<li>It is a stippled blue line seen in 50-70% of patients with chronic lead poisoning</li>
<li>It is manifested as a bluish black line due to epidermal deposition of lead sulphate at the junction of the gums with the teeth (not seen on the teeth)</li>
<li>Similar pigmented lines are seen in poisoning with mercury, copper, silver, bismuth and iron poisoning</li>
<li>Other features of chronic lead poisoning include pallor (anemia), constipation, paralysis and lead encephalopathy</li>
</ul>
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		<title>Hyperlipidemia in nephrotic syndrome – Mechanism</title>
		<link>http://pgblazer.com/2010/11/hyperlipidemia-in-nephrotic-syndrome-mechanism.html</link>
		<comments>http://pgblazer.com/2010/11/hyperlipidemia-in-nephrotic-syndrome-mechanism.html#comments</comments>
		<pubDate>Tue, 30 Nov 2010 00:52:51 +0000</pubDate>
		<dc:creator>pgblazer</dc:creator>
				<category><![CDATA[Featured]]></category>
		<category><![CDATA[Medicine]]></category>
		<category><![CDATA[Nephrology]]></category>
		<category><![CDATA[Pathology]]></category>

		<guid isPermaLink="false">http://pgblazer.com/?p=3575</guid>
		<description><![CDATA[

Diabetes glomerulosclerosis with nephrotic syndrome &#8211; histopathology
Click on image for an enlarged view

Nephrotic syndrome is characterised by albuminuria, hypoalbuminemia, oedema, hyperlipidemia and lipiduria
The increased loss of proteins in urine stimulates the liver to increase synthesis of proteins
Apolipoporteins are synthesised in increased quantities &#8211; especially apo B, apo C-II, and apo E which are used VLDL and LDL formation
Apoproteins associated with HDL synthesis &#8211; apo A-I and apo A-II usually remains normal
In addition to this, there is decreased lipid catabolism due to decreased activity of lipoprotein lipase
All these factors together contribute ...   
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			<content:encoded><![CDATA[<h5 style="text-align: center;"><a href="http://d36i1lch6ipbwf.cloudfront.net/wp-content/uploads/2010/11/Diabetic-glomerulosclerosis.jpg" rel="lightbox[3575]"><br />
<img class="aligncenter size-medium wp-image-3577" title="Diabetes glomerulosclerosis with nephrotic syndrome" src="http://d36i1lch6ipbwf.cloudfront.net/wp-content/uploads/2010/11/Diabetic-glomerulosclerosis-300x225.jpg" alt="" width="300" height="225" /></a><br />
Diabetes glomerulosclerosis with nephrotic syndrome &#8211; histopathology<br />
Click on image for an enlarged view</h5>
<ul>
<li>Nephrotic syndrome is characterised by albuminuria, hypoalbuminemia, oedema, hyperlipidemia and lipiduria</li>
<li>The increased loss of proteins in urine stimulates the liver to increase synthesis of proteins</li>
<li><strong>Apolipoporteins are synthesised in increased quantities</strong> &#8211; especially apo B, apo C-II, and apo E which are used VLDL and LDL formation</li>
<li>Apoproteins associated with HDL synthesis &#8211; apo A-I and apo A-II usually remains normal</li>
<li>In addition to this, there is<strong> decreased lipid catabolism </strong>due to decreased activity of lipoprotein lipase</li>
<li>All these factors together contribute to the hyperlipidemic state in nephrotic syndrome</li>
</ul>
<h5 style="text-align: left;"><a href="http://en.wikipedia.org/wiki/File:Diabetic_glomerulosclerosis_(1)_HE.jpg" rel="lightbox[3575]"><span style="font-weight: normal;">Image source</span></a></h5>
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		<title>Allergic mediators released from mast cells</title>
		<link>http://pgblazer.com/2010/09/allergic-mediators-released-from-mast-cells.html</link>
		<comments>http://pgblazer.com/2010/09/allergic-mediators-released-from-mast-cells.html#comments</comments>
		<pubDate>Fri, 03 Sep 2010 04:15:46 +0000</pubDate>
		<dc:creator>pgblazer</dc:creator>
				<category><![CDATA[Pathology]]></category>

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		<description><![CDATA[Antigens can cause degranulation of mast cells resulting in allergic reactions. Some of the allergic mediators released from mast cells are preformed whereas others are synthesised on demand.



Preformed   mediators



ECF-A
Eosinophil   chemotactic factor  of Anaphylaxis &#8211;   attracts eosinophils to the site


NCF &#8211; A
Neutrophil   chemotactic factor &#8211; attracts neutrophils to the site


Histamine
Vasodilation and   bronchospasm


Heparin
Promotes   phagocytosis


Newly synthesised   mediators



Prostaglandin
Vasoconstriction   and bronchospasm


Leukotriene
Vasoconstriction   and bronchospasm


Thromboxane A2
Vasoconstriction   and platelet aggregation


PAF
Platelet   Activating Factor &#8211; bronchospasm, platelet aggregation, ...   
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			<content:encoded><![CDATA[<p>Antigens can cause degranulation of mast cells resulting in allergic reactions. Some of the allergic mediators released from mast cells are preformed whereas others are synthesised on demand.</p>
<table>
<tbody>
<tr>
<th>Preformed   mediators</th>
<th></th>
</tr>
<tr>
<td>ECF-A</td>
<td>Eosinophil   chemotactic factor  of Anaphylaxis &#8211;   attracts eosinophils to the site</td>
</tr>
<tr>
<td>NCF &#8211; A</td>
<td>Neutrophil   chemotactic factor &#8211; attracts neutrophils to the site</td>
</tr>
<tr>
<td>Histamine</td>
<td>Vasodilation and   bronchospasm</td>
</tr>
<tr>
<td>Heparin</td>
<td>Promotes   phagocytosis</td>
</tr>
<tr>
<th>Newly synthesised   mediators</th>
<th></th>
</tr>
<tr>
<td>Prostaglandin</td>
<td>Vasoconstriction   and bronchospasm</td>
</tr>
<tr>
<td>Leukotriene</td>
<td>Vasoconstriction   and bronchospasm</td>
</tr>
<tr>
<td>Thromboxane A2</td>
<td>Vasoconstriction   and platelet aggregation</td>
</tr>
<tr>
<td>PAF</td>
<td>Platelet   Activating Factor &#8211; bronchospasm, platelet aggregation, chemotaxis of   neutrophils, eosinophils</td>
</tr>
<tr>
<td>TNF alpha</td>
<td>Tumour necrosis   factor &#8211; transmigration of eosinophils and neutrophils</td>
</tr>
</tbody>
</table>
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                     <img src="http://d36i1lch6ipbwf.cloudfront.net/wp-content/themes/arthemia/default-image.jpg" alt="Alpha-2 adrenergic receptor &#8211; Location, Actions, Agonist, Antagonists" width="100px" height="100px"  />  
                   
   
                 Alpha-2 adrenergic receptor &#8211; Location, Actions, Agonist, Antagonists</a>  
             </li>  
   
           
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		</item>
		<item>
		<title>Ballooning degeneration</title>
		<link>http://pgblazer.com/2009/11/ballooning-degeneration.html</link>
		<comments>http://pgblazer.com/2009/11/ballooning-degeneration.html#comments</comments>
		<pubDate>Wed, 04 Nov 2009 13:34:58 +0000</pubDate>
		<dc:creator>pgblazer</dc:creator>
				<category><![CDATA[Pathology]]></category>
		<category><![CDATA[apoptosis]]></category>
		<category><![CDATA[ballooning]]></category>
		<category><![CDATA[Ballooning degeneration]]></category>
		<category><![CDATA[cytoplasmic vacuolation]]></category>
		<category><![CDATA[hepatocyte]]></category>
		<category><![CDATA[hepatocyte death]]></category>
		<category><![CDATA[pyknotic nucleus]]></category>
		<category><![CDATA[viruses]]></category>

		<guid isPermaLink="false">http://www.pgblazer.com/?p=1492</guid>
		<description><![CDATA[
Ballooning degeneration of hepatocytes
(Click on image for an enlarged view &#8211; Image by Nephron)

Type of hepatocyte death
Form of apoptosis
Seen in hepatocytes infected with certain viruses
characterised by increase in cell size (ballooning) with wispy/cobweb like cytoplasm, cytoplasmic vacuolation, pyknotic nucleus

   
 
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			<content:encoded><![CDATA[<p style="text-align: center;"><a title="Ballooning degeneration of hepatocytes" href="http://d36i1lch6ipbwf.cloudfront.net/wp-content/uploads/2009/11/Ballooning_degeneration_high_mag1.jpg" rel="lightbox[1492]"><img class="aligncenter size-full wp-image-1493" title="Ballooning degeneration" src="http://d36i1lch6ipbwf.cloudfront.net/wp-content/uploads/2009/11/Ballooning_degeneration-580px.jpg" alt="Ballooning degeneration" width="580" height="387" /></a></p>
<h3 style="text-align: center;">Ballooning degeneration of hepatocytes</h3>
<h5 style="text-align: center;">(Click on image for an enlarged view &#8211; Image by <a href="http://commons.wikimedia.org/wiki/User:Nephron" target="_blank">Nephron</a>)</h5>
<ul>
<li>Type of hepatocyte death</li>
<li>Form of apoptosis</li>
<li>Seen in hepatocytes infected with certain viruses</li>
<li>characterised by increase in cell size (ballooning) with wispy/cobweb like cytoplasm, cytoplasmic vacuolation, pyknotic nucleus</li>
</ul>
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		<item>
		<title>Causes of renal papillary necrosis</title>
		<link>http://pgblazer.com/2009/11/causes-of-renal-papillary-necrosis.html</link>
		<comments>http://pgblazer.com/2009/11/causes-of-renal-papillary-necrosis.html#comments</comments>
		<pubDate>Wed, 04 Nov 2009 12:03:47 +0000</pubDate>
		<dc:creator>pgblazer</dc:creator>
				<category><![CDATA[Pathology]]></category>
		<category><![CDATA[Analgesic nephropathy]]></category>
		<category><![CDATA[calcification]]></category>
		<category><![CDATA[Diabetes mellitus]]></category>
		<category><![CDATA[Obstruction]]></category>
		<category><![CDATA[papillary necrosis]]></category>
		<category><![CDATA[renal papillary necrosis]]></category>
		<category><![CDATA[Sickle cell disease]]></category>

		<guid isPermaLink="false">http://www.pgblazer.com/?p=1489</guid>
		<description><![CDATA[
Diabetes mellitus &#8211; several papillae affected, all of same stage, rarely calcify
Analgesic nephropathy &#8211; almost all papillae affected, different stage of necrosis,calcification frequent
Sickle cell disease &#8211; few papillae affected, rarely calcify
Obstruction &#8211; variable number of papillae affected, calcification frequent

   
 
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 ]]></description>
			<content:encoded><![CDATA[<ul>
<li>Diabetes mellitus &#8211; several papillae affected, all of same stage, rarely calcify</li>
<li>Analgesic nephropathy &#8211; almost all papillae affected, different stage of necrosis,calcification frequent</li>
<li>Sickle cell disease &#8211; few papillae affected, rarely calcify</li>
<li>Obstruction &#8211; variable number of papillae affected, calcification frequent</li>
</ul>
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		<title>Kveim test</title>
		<link>http://pgblazer.com/2009/11/kveim-test.html</link>
		<comments>http://pgblazer.com/2009/11/kveim-test.html#comments</comments>
		<pubDate>Wed, 04 Nov 2009 11:56:15 +0000</pubDate>
		<dc:creator>pgblazer</dc:creator>
				<category><![CDATA[Pathology]]></category>
		<category><![CDATA[bovine spongiform encephalopathy]]></category>
		<category><![CDATA[granulomas]]></category>
		<category><![CDATA[Kveim antigen]]></category>
		<category><![CDATA[Kveim Nickerson skin test]]></category>
		<category><![CDATA[Kveim test]]></category>
		<category><![CDATA[Morten Ansgar Kveim]]></category>
		<category><![CDATA[Nickerson Kveim reaction]]></category>
		<category><![CDATA[sarcoidosis]]></category>

		<guid isPermaLink="false">http://www.pgblazer.com/?p=1482</guid>
		<description><![CDATA[
Skin test to detect sarcoidosis
Intracutaneous injection of spleen extract of patient with sarcoidosis (Kveim antigen)
Positive result &#8211; granulomas found 4-6 weeks later
False negative &#8211; corticosteroid therapy
Risk of transmission of diseases like bovine spongiform encephalopathy- hence not done nowadays
Named after norwegian pathologist Morten Ansgar Kveim

Also called:

Nickerson Kveim reaction
Kveim Nickerson skin test

   
 
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			<content:encoded><![CDATA[<ul>
<li>Skin test to detect sarcoidosis</li>
<li>Intracutaneous injection of spleen extract of patient with sarcoidosis (Kveim antigen)</li>
<li>Positive result &#8211; granulomas found 4-6 weeks later</li>
<li>False negative &#8211; corticosteroid therapy</li>
<li>Risk of transmission of diseases like bovine spongiform encephalopathy- hence not done nowadays</li>
<li>Named after norwegian pathologist Morten Ansgar Kveim</li>
</ul>
<p>Also called:</p>
<ul>
<li>Nickerson Kveim reaction</li>
<li>Kveim Nickerson skin test</li>
</ul>
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		<title>Karyotyping</title>
		<link>http://pgblazer.com/2009/06/karyotyping.html</link>
		<comments>http://pgblazer.com/2009/06/karyotyping.html#comments</comments>
		<pubDate>Tue, 09 Jun 2009 18:03:21 +0000</pubDate>
		<dc:creator>admin2</dc:creator>
				<category><![CDATA[Pathology]]></category>

		<guid isPermaLink="false">http://www.pgblazer.com/?p=1241</guid>
		<description><![CDATA[Karyotyping is a method for studying the chromosomes of an organizm. Karyotype is a standardised arrangement of metaphasic chromosomes that have been photographed and arranged in the order of decreasing length. The cell division is arrested in metaphase by using inhibitors of spindle formation like colchicine and stained. Different techniques for staining are available to identify the individual chromosomes eg. staining with Giemsa (G bandng). G banding shows alternating dark and light bands in the chromosome. Numerical chromosomal abnormalities such as trisomy 21 (Down syndrome) can be easily identified using ...   
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			<content:encoded><![CDATA[<p>Karyotyping is a method for studying the chromosomes of an organizm. Karyotype is a standardised arrangement of metaphasic chromosomes that have been photographed and arranged in the order of decreasing length. The cell division is arrested in metaphase by using inhibitors of spindle formation like colchicine and stained. Different techniques for staining are available to identify the individual chromosomes eg. staining with Giemsa (G bandng). G banding shows alternating dark and light bands in the chromosome. Numerical chromosomal abnormalities such as trisomy 21 (Down syndrome) can be easily identified using karyotyping. One disadvantage is that karyotyping can be applied only to cells which divide or can be induced to divide in vitro. </p>
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		<title>Hyaline change</title>
		<link>http://pgblazer.com/2009/06/hyaline-change.html</link>
		<comments>http://pgblazer.com/2009/06/hyaline-change.html#comments</comments>
		<pubDate>Tue, 09 Jun 2009 17:51:16 +0000</pubDate>
		<dc:creator>admin2</dc:creator>
				<category><![CDATA[Pathology]]></category>

		<guid isPermaLink="false">http://www.pgblazer.com/?p=1238</guid>
		<description><![CDATA[Hyaline change is a homogenous glassy pink appearance in the histological sections stained with hematoxylin and eosin. It can be due to intracellular accumulation of certain substances as in Russel bodies (multiple myeloma), Mallory bodies (alcoholic liver disease), re-absorption droplets (kidney). Extra cellular hyaline change can be seen in walls of the arterioles in long standing hypertension and diabetes mellitus. This is due to extravasated plasma protein and deposition of basement membrane material.
   
 
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			<content:encoded><![CDATA[<p>Hyaline change is a homogenous glassy pink appearance in the histological sections stained with hematoxylin and eosin. It can be due to intracellular accumulation of certain substances as in Russel bodies (multiple myeloma), Mallory bodies (alcoholic liver disease), re-absorption droplets (kidney). Extra cellular hyaline change can be seen in walls of the arterioles in long standing hypertension and diabetes mellitus. This is due to extravasated plasma protein and deposition of basement membrane material.</p>
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		<title>Anticoagulants and their uses</title>
		<link>http://pgblazer.com/2009/06/anticoagulants-and-their-uses.html</link>
		<comments>http://pgblazer.com/2009/06/anticoagulants-and-their-uses.html#comments</comments>
		<pubDate>Tue, 09 Jun 2009 17:42:58 +0000</pubDate>
		<dc:creator>admin2</dc:creator>
				<category><![CDATA[Pathology]]></category>

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		<description><![CDATA[The commonly used anticoagulants are: heparin, citrate, oxalate, EDTA. Citrate is used for the storage of blood. Heparin is for taking blood samples for ABG estimation. Oxalate and EDTA are used while collecting blood for investigation. 
   
 
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			<content:encoded><![CDATA[<p>The commonly used anticoagulants are: heparin, citrate, oxalate, EDTA. Citrate is used for the storage of blood. Heparin is for taking blood samples for ABG estimation. Oxalate and EDTA are used while collecting blood for investigation. </p>
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		<title>Types of infarcts</title>
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		<pubDate>Tue, 09 Jun 2009 17:36:47 +0000</pubDate>
		<dc:creator>admin2</dc:creator>
				<category><![CDATA[Pathology]]></category>

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		<description><![CDATA[Infarcts can be classified into red (hemorarragic) white (anemic) infarcts as well as septic and bland infarcts. Red infarcts can occur in lungs while infarcts occur in the heart, kidney and spleen. Septic infarcts can occur when a vegetation of infective endocarditis embolises. 
   
 
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			<content:encoded><![CDATA[<p>Infarcts can be classified into red (hemorarragic) white (anemic) infarcts as well as septic and bland infarcts. Red infarcts can occur in lungs while infarcts occur in the heart, kidney and spleen. Septic infarcts can occur when a vegetation of infective endocarditis embolises. </p>
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		<title>Fatty change</title>
		<link>http://pgblazer.com/2009/06/fatty-change.html</link>
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		<pubDate>Tue, 09 Jun 2009 17:28:00 +0000</pubDate>
		<dc:creator>admin2</dc:creator>
				<category><![CDATA[Pathology]]></category>

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		<description><![CDATA[Fatty change is the accumulation of lipid droplets within the parenchymal cells. It usually occurs in the liver as the liver has great involvement in fat metabolism. Other organs in which fatty change can occur are the heart and muscle. Causes of fatty change may be hypoxia, exposure to toxins like carbon tetra chloride, obesity, protein malnutrition, diabetes mellitus. The most common cause of fatty change of liver is alcoholic fatty liver. Non alcoholic steatosis and non alcoholic steatohepatitis are being increasingly seen now a days. Accumulation of fat in ...   
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			<content:encoded><![CDATA[<p>Fatty change is the accumulation of lipid droplets within the parenchymal cells. It usually occurs in the liver as the liver has great involvement in fat metabolism. Other organs in which fatty change can occur are the heart and muscle. Causes of fatty change may be hypoxia, exposure to toxins like carbon tetra chloride, obesity, protein malnutrition, diabetes mellitus. The most common cause of fatty change of liver is alcoholic fatty liver. Non alcoholic steatosis and non alcoholic steatohepatitis are being increasingly seen now a days. Accumulation of fat in the liver can occur due to derangement of any of the processes from uptake of fatty acids to the release of triglycerides. </p>
<p>Fat metabolism in the liver </p>
<p>Lipids absorbed in the intestine are transported to the liver by the portal circulation where they are taken up by the hepatocytes. These fatty acids can be 1) oxidized to ketone bodies 2) used for the synthesis of cholesterol 3) used for synthesis of triglycerides. </p>
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		<title>Myelodysplastic syndrome (MDS)</title>
		<link>http://pgblazer.com/2009/05/myelodysplastic-syndrome-mds.html</link>
		<comments>http://pgblazer.com/2009/05/myelodysplastic-syndrome-mds.html#comments</comments>
		<pubDate>Sun, 31 May 2009 08:28:56 +0000</pubDate>
		<dc:creator>admin2</dc:creator>
				<category><![CDATA[Medicine]]></category>
		<category><![CDATA[Pathology]]></category>

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		<description><![CDATA[It is a heterogenous group of conditions with cytopenias, hypercellular / dysplastic marrow and is a premalignant condition. Dyserythropoesis manifest as ring sideroblasts. 
In MDS, there is decreased normal hemopoetic stem cells, proliferation of dyspoetic marrow cells, selective outgrowth of MDS cells and malignant transformation. 
Most patients with MDS die of cytopenias than of leukemia. Transfusion dependence is also an important prognostic factor in MDS. Those who need more transfusions have a poorer prognosis. 
5q deletion (5q minus) syndrome has been identified as an important factor in MDS, but this ...   
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			<content:encoded><![CDATA[<p>It is a heterogenous group of conditions with cytopenias, hypercellular / dysplastic marrow and is a premalignant condition. Dyserythropoesis manifest as ring sideroblasts. </p>
<p>In MDS, there is decreased normal hemopoetic stem cells, proliferation of dyspoetic marrow cells, selective outgrowth of MDS cells and malignant transformation. </p>
<p>Most patients with MDS die of cytopenias than of leukemia. Transfusion dependence is also an important prognostic factor in MDS. Those who need more transfusions have a poorer prognosis. </p>
<p>5q deletion (5q minus) syndrome has been identified as an important factor in MDS, but this group does not go in for a malignant transformation.</p>
<p>Classifications: FAB (1982) and WHO (2001) classifications</p>
<p>IPSS risk score for de novo MDS is based on marrow blasts, karyotype and cytopenias. Refractory anemia sub group has a lower risk.</p>
<p><strong>Treatment of myelodysplastic syndrome:</strong></p>
<p>Packed cells – but this can cause iron overload, which occurs when you give more than 40 transfusions. Desferrioxamine has to be given to prevent hemochromatosis due to iron overload.</p>
<p>Erythopoetin is a worth a try, even though the response rates are only 20 &#8211; 30%. Darbepoetin is a syntetic analogue, which is not freely available. Thrombopoetin in addition to platelet transfusion can be used. </p>
<p>Lenalidomide, a congener of thalidomide and induces an erythroid response in about 50%. Response to lenalidomide is better in 5q minus syndrome.</p>
<p>Hypomethylating agent 5-Azactytidine is also useful. Time to AML or death is increased with this drug.</p>
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		<title>Hurthle cells or Askanazy cells</title>
		<link>http://pgblazer.com/2009/05/hurthle-cells-or-askanazy-cells.html</link>
		<comments>http://pgblazer.com/2009/05/hurthle-cells-or-askanazy-cells.html#comments</comments>
		<pubDate>Sun, 31 May 2009 07:34:38 +0000</pubDate>
		<dc:creator>admin2</dc:creator>
				<category><![CDATA[Pathology]]></category>

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		<description><![CDATA[Hurthle cells or Askanazy cells seen in Hashimoto&#8217;s thyroiditis.
   
 
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			<content:encoded><![CDATA[<p>Hurthle cells or Askanazy cells seen in Hashimoto&#8217;s thyroiditis.</p>
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		<title>Haemophilus influenzae</title>
		<link>http://pgblazer.com/2009/02/haemophilus-influenzae.html</link>
		<comments>http://pgblazer.com/2009/02/haemophilus-influenzae.html#comments</comments>
		<pubDate>Mon, 09 Feb 2009 07:16:40 +0000</pubDate>
		<dc:creator>pgblazer</dc:creator>
				<category><![CDATA[Microbiology]]></category>
		<category><![CDATA[Pathology]]></category>

		<guid isPermaLink="false">http://www.pgblazer.com/?p=645</guid>
		<description><![CDATA[It is a small gram negative bacillus.
 

Haemophilus influenzae in blood agar
Haemophilus influenzae meningitis
   
 
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			<content:encoded><![CDATA[<p>It is a small gram negative bacillus.</p>
<p> </p>
<p><img class="aligncenter size-medium wp-image-647" title="Haemophilus influenzae" src="http://d36i1lch6ipbwf.cloudfront.net/wp-content/uploads/2009/02/800px-haemophilus_influenzae_01-300x202.jpg" alt="Haemophilus influenzae" width="300" height="202" /></p>
<h5 style="text-align: center;">Haemophilus influenzae in blood agar</h5>
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		<title>Malignancies of the oesophagus show early lymphatic spread because</title>
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		<pubDate>Fri, 06 Feb 2009 02:05:42 +0000</pubDate>
		<dc:creator>pgblazer</dc:creator>
				<category><![CDATA[Pathology]]></category>

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		<description><![CDATA[Oesophagus has rich longitudinaly running lymphatics which facilitate metastatic spread. Also oesphagus is the only area of the GIT which has no serosal covering which is also favourable for metastais.
   
 
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			<content:encoded><![CDATA[<p>Oesophagus has rich longitudinaly running lymphatics which facilitate metastatic spread. Also oesphagus is the only area of the GIT which has no serosal covering which is also favourable for metastais.</p>
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		<pubDate>Thu, 05 Feb 2009 11:10:11 +0000</pubDate>
		<dc:creator>pgblazer</dc:creator>
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			<content:encoded><![CDATA[<p>Destruction of RBS&#8217;s with release of hemoglobin and other red cell contents into the plasma.</p>
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		<title>Hemoglobinemia</title>
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		<pubDate>Thu, 05 Feb 2009 11:08:11 +0000</pubDate>
		<dc:creator>pgblazer</dc:creator>
				<category><![CDATA[Pathology]]></category>

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			<content:encoded><![CDATA[<p>Presence of excess hemoglobin in plasma. Normally hemoglobin is located within the red blood cells. When there is increased hemolysis, hemoglobin is rapidly released into the plasma resulting in hemoglobinemia.</p>
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