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      <title>Pancreatic insufficiency  by </title>
      <link>https://padlet.com/manarmech/Bookmarks</link>
      <description>Made with fortitude</description>
      <language>en-us</language>
      <pubDate>2022-01-30 21:14:24 UTC</pubDate>
      <lastBuildDate>2022-03-09 14:34:48 UTC</lastBuildDate>
      <webMaster>hello@padlet.com</webMaster>
      <image>
         <url></url>
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      <item>
         <title>Acute pancreatitis</title>
         <author>manarmech</author>
         <link>https://padlet.com/manarmech/Bookmarks/wish/2058252055</link>
         <description><![CDATA[<div>= A syndrome of inflammation of the pancreatic gland initiation by an acute injury</div><ul><li>Gallstones and alcohol are the major causes (in Western world)</li><li>Severity of pancreatitis may range from mild and self-limiting to extremely severe, with extensive pancreatic and peripancreatic necrosis as well as haemorrhage.</li><li>In the most severe cases (10%), mortality is between 40-50%</li><li><strong>Pathogenesis</strong><ul><li>The pancreatic inflammatory response is secondary to the premature exaggerated activation of digestives enzymes within the pancreas itself</li><li>An acute rise in intracellular calcium may be the initiating mechanism, leading to early activation of trypsinogen to trypsin and impairment of trypsin degradation by chymotrypsin C</li><li>These activated enzymes are responsible for cellular necrosis</li><li>In the case of gallstone-related pancreatitis it is believed that stones occlude the pancreatic drainage at the level of the ampulla leading to pancreatic ductular hypertension, which increases cytosolic free ionised calcium&nbsp;</li><li>Alcohol interferes with calcium homeostasis in pancreatic acinar cells</li></ul></li><li><strong>Clinical features</strong><ul><li>Acute pancreatitis is DD in any patient with upper abdominal pain (stabbing)&nbsp;</li><li>The pain usually begins in the epigastrium accompanied by nausea and vomiting</li><li>As inflammation spreads through the peritoneal cavity, the pain becomes more intense</li><li>Involvement of the retroperitoneum frequently leads to back pain</li></ul></li><li>&nbsp;<strong>Diagnosis</strong><ul><li>Blood tests<ul><li><em>Serum amylase</em></li><li><em>Urinary amylase</em></li><li><em>Serum lipase</em></li><li><em>C-reactive protein level</em></li><li><em>Erect chest X-ray</em></li><li><em>Abdominal ultrasound scan</em></li><li><em>Contrast-enhanced CT scanning</em></li><li><em>MRI (MRCP)</em></li><li><em>ERCP</em></li></ul></li></ul></li><li><strong>Assessment&nbsp;</strong><ul><li>Majority of cases are mild and run a short, self-limiting course</li><li>25% run a more complicated course</li><li>10% may be life-threatening&nbsp;</li><li>haemodynamic instability and multiple organ failure&nbsp;</li><li>Early clinical assessment has been shows to have poor sensitivity for predicting a severe attack&nbsp;</li><li>Ranson and Glasgow scoring system</li><li>Acute physiology and chronic health evaluation (APACHE) score</li></ul></li><li><strong>treatment</strong><ul><li><em>Nasogastric suction</em>: prevents abdominal distension and vomitus and hence the risk of pneumonia&nbsp;</li><li><em>Baseline arterial blood gases</em>: key predictive factor for severity of an episode and determine the need for continuous oxygen administration</li><li><em>Prophylactic antibiotics</em>: unknown how useful it is. There is evidence that the beta lactam imipenem reduced the incidence of infected pancreatic necrosis</li><li><em>Analgesia requirements</em>: opiates are the drug of choice for immediate post-presentation pain control.&nbsp;</li><li><em>Feeding</em>: in patients with a severe episode there is little likelihood of oral nutrition for a number of weeks. Total parenteral nutrition is associated with a high risk of infection and has been replaced by enteral nutrition</li><li><em>Anticoagulation</em>: with low molecular weight heparin for DVT prophylaxis</li></ul></li><li><strong>complications</strong><ul><li>reflection on the systemic inflammatory response, which in turn results in multiple organ failure</li><li>After this initial period, the prognosis is mostly related to the extent of pancreatic necrosis</li><li>When the damaged area has been walled off and liquefaction has begun and pseudocyst develops</li><li>acute sepsis&nbsp;</li></ul></li><li><strong>prognosis</strong><ul><li>full recovery mild to moderate AP</li><li>recurrent episodes&nbsp;</li><li>insufficient exocrine and endocrine function in sever AP</li></ul></li></ul><div><br></div><div><br></div>]]></description>
         <enclosure url="" />
         <pubDate>2022-02-21 07:24:36 UTC</pubDate>
         <guid>https://padlet.com/manarmech/Bookmarks/wish/2058252055</guid>
      </item>
      <item>
         <title>Chronic pancreatitis</title>
         <author>manarmech</author>
         <link>https://padlet.com/manarmech/Bookmarks/wish/2058252301</link>
         <description><![CDATA[<div><strong>Aetiology</strong></div><ul><li>Developed countries: 60-80% alcohol is cause</li><li>Other factors: toxic-metabolic, genetic, autoimmune, recurrent acute or severe acute pancreatitis, obstruction and idiopathic&nbsp;</li></ul><div><strong>Pathogenesis</strong></div><ul><li>An increase in activated trypsin within the pancreas is a common pathway for the development of chronic pancreatitis<ul><li>result of increased/premature activation of trypsinogen to trypsin or by imapred inactivation/clearance of the activated enzyme of the pancreas</li><li>Increased/prolonged intrapancreatic enzyme activity leads to the precipitation of proteins within the duct lumen inthe form of plugs</li><li>These form a nidus for calcification and are the cause of ductal obstruction leading to ductal hypertension and further pancreatic damage</li></ul></li><li><em>Alcohol related chronic pancreatitis&nbsp;</em><ul><li>Alcohol impairs calcium regulation leading to increased levels</li><li>These promote trypsinogen activation and diminish the inactivation pathway</li><li>Alcohol is only one factor which interacts with other environmental/genetic influences</li></ul></li><li><em>genetics aspects</em><ul><li>trypsinogen produced in the pancreas and encoded by the PRSS1 gene --&gt; mutated&nbsp;</li><li>SPINK-1 is a specific trypsin inhibitor and is co-secreted with trypsinogen by the acinar cells. Loss of function mutations of SPINK-1 gene&nbsp;</li><li>Chymotrypsin C is produced in trace amounts by the acinar cells and has a role in trypsin inactivation. Loss of function mutations of the encoding gene&nbsp;</li><li>CFTR mutation → idiopathic chronic pancreatitis</li></ul></li><li><em>Autoimmune chronic pancreatitis (ACP)</em><ul><li>IgG4-related disorders: include autoimmune cholangitis, Reidel’s thyroiditis, aortitis and tubulo-interstitial nephritis.&nbsp;</li></ul></li></ul><div><strong>clinical features</strong></div><ul><li>pain, usually epigastric and often radiates through into the back</li><li>&nbsp;episodic, with short periods of severe pain, or chronic unremitting Exacerbations</li><li>abdominal pain anorexia is common and weight loss may be severe</li><li>Exocrine and endocrine insufficiency&nbsp;</li><li>Jaundice&nbsp;</li></ul><div><strong>investigation&nbsp;</strong></div><ul><li>Serum amylase and lipase:&nbsp; elevated</li><li>Faecal elastase: abnormal&nbsp;</li><li>Gene mutation analysis</li><li>Transabdominal ultrasound scan</li><li>Contrast-enhanced spiral CT scan</li><li>MRI and MRCP</li><li>Endoscopic ultrasound:</li></ul><div><strong>Differential diagnosis</strong></div><ul><li>Carcinoma of the pancreas&nbsp;</li><li>The diagnosis of malignancy should be considered in patients with short history and in whom there is a localised ductular abnormality</li></ul><div><strong>treatment</strong></div><ul><li><strong>s</strong>hort-term flare-ups of pain a combination of non-steroidal anti-inflammatory drug and an opiate for abdominal pain&nbsp;</li><li>&nbsp;pancreatic enzyme supplements steatorrhoea&nbsp;</li><li>treat diabetes&nbsp;</li></ul><div><strong>complications</strong></div><ul><li>Pseudocyst = fluid collection surrounded by granulation tissue (most common structural complication)</li><li>Ascites and occasionally pleural effusions</li><li>Cystic fibrosis</li><li>Increased risk of pancreatic cancer</li></ul><div><br></div>]]></description>
         <enclosure url="" />
         <pubDate>2022-02-21 07:24:49 UTC</pubDate>
         <guid>https://padlet.com/manarmech/Bookmarks/wish/2058252301</guid>
      </item>
      <item>
         <title>Cystic tumors</title>
         <author>manarmech</author>
         <link>https://padlet.com/manarmech/Bookmarks/wish/2058253678</link>
         <description><![CDATA[<ul><li><strong>Serous cystadenomas</strong><ul><li>composed of multiple small cystic cavities lined by cuboidal glycogen-rich, mucin-poor cells.&nbsp;</li><li>elderly age group, asymptomatic&nbsp;</li><li>Malignant transformation in a serous cystadenoma is extremely rare. Larger serous cystadenomas may cause local compressive complications</li></ul></li><li><strong>Mucinous cystadenomas</strong><ul><li>&nbsp;exclusively found in women in the 5th and 6th decades and are sited in the pancreatic body and tail.</li><li>Multilocular cysts are lined by tall mucin-synthesising cells.&nbsp;</li><li>20% are malignant at the time of presentation and the majority appear to have a malignant potential. more likely to produce symptoms.</li></ul></li><li><strong>Intraductal papillary mucinous tumour (IPMT)</strong><strong><em>&nbsp;</em></strong><ul><li>pancreatic cystic neoplasm that can arise from either the side branches or the main duct.&nbsp;</li><li>the majority are found in men 60-70.</li><li>pancreatic pain/asymptomatic.&nbsp;</li><li>slowly progressive with a significant malignant potential; more so when the main duct is the site of origin.</li></ul></li></ul>]]></description>
         <enclosure url="" />
         <pubDate>2022-02-21 07:25:47 UTC</pubDate>
         <guid>https://padlet.com/manarmech/Bookmarks/wish/2058253678</guid>
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      <item>
         <title>Neuroendocrine tumours</title>
         <author>manarmech</author>
         <link>https://padlet.com/manarmech/Bookmarks/wish/2058253997</link>
         <description><![CDATA[<div>heterogeneous group of tumours with varying tumour biology and prognosis and 40–50% of the patients present with symptoms related to the substances released from the tumours</div><ul><li>&nbsp;<strong>Investigation and management</strong><ul><li>cross-sectional imaging, including CT and MRI scanning. Expression of <strong>somatostatin receptors</strong> and can be mapped by scintigraphy. Recently, PET scanning with specific isotopes have been introduced.</li><li>surgery of the primary lesion</li><li>Somatostatin analogues  to control hormonal related symptoms and also have a tumour modulating effect.,</li></ul></li><li><strong>Presentation</strong><ul><li>Endoscopic ultrasound most sensitive means of detecting small tumours. Many of these tumours have somatostatin receptors, and radiolabeled somatostatin analogue scanning provides a means of tumour localization.</li></ul></li><li><strong>Treatment</strong><ul><li><em>Surgical resection </em>of the pancreatic lesion is the only potential curative approach</li><li>Somatostatin analogues</li><li>antiangiogenesis therapy utilising vascular endothelial growth factor (VEGF) antagonists</li></ul></li></ul>]]></description>
         <enclosure url="" />
         <pubDate>2022-02-21 07:26:03 UTC</pubDate>
         <guid>https://padlet.com/manarmech/Bookmarks/wish/2058253997</guid>
      </item>
      <item>
         <title>Jaundice</title>
         <author>manarmech</author>
         <link>https://padlet.com/manarmech/Bookmarks/wish/2058254392</link>
         <description><![CDATA[<div>&nbsp;types of jaundice</div><ul><li>Jaundice (icterus) is detectable clinically when the serum bilirubin is &gt;50 μmol/L (3 mg/dL).<ul><li>Haemolytic jaundice – increased bilirubin load for the liver cells</li><li>Congenital hyperbilirubinemias – defects in conjugation<ul><li>Unconjugated<ul><li>Gilbert’s syndrome, Crigler–Najjar syndrome</li></ul></li><li>Conjugated<ul><li>Benign recurrent intrahepatic cholestasis, Progressive familial intrahepatic cholestasis (PFIC) syndromes</li></ul></li></ul></li><li>Cholestatic jaundice, including hepatocellular (parenchymal) liver disease and large duct obstruction.</li></ul></li></ul><div>Differential diagnosis of jaundice</div><ul><li>history</li></ul><div>clinical features&nbsp;</div><ul><li>signs of acute and chronic liver disease:<ul><li><strong>Hepatomegaly</strong>.&nbsp;<ul><li>A smooth tender liver is seen in hepatitis and with extrahepatic obstruction, but a knobbly irregular liver suggests metastases.&nbsp;</li></ul></li><li><strong>Splenomegaly</strong>.<ul><li>&nbsp;This indicates portal hypertension in patients when signs of chronic liver disease are present. The spleen can also be ‘tipped’ occasionally in viral hepatitis.</li></ul></li><li><strong>Ascites</strong><em>.</em><ul><li>&nbsp;This is found in cirrhosis but can also be due to carcinoma (particularly ovarian) and many other causes&nbsp;</li></ul></li></ul></li><li>palpable gallbladder occurs with a carcinoma of the pancreas obstructing the bile duct</li><li>Cold sores are seen with a herpes simplex virus hepatitis.</li></ul><div>investigations</div><ul><li>ultrasound<ul><li>size bile duct, level obstruction</li></ul></li><li>liverbiochemistry<ul><li>AST/ALT</li></ul></li><li>haematology<ul><li>WBC, mononuclear cells&nbsp;</li></ul></li></ul><div><br></div>]]></description>
         <enclosure url="" />
         <pubDate>2022-02-21 07:26:20 UTC</pubDate>
         <guid>https://padlet.com/manarmech/Bookmarks/wish/2058254392</guid>
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      <item>
         <title></title>
         <author>manarmech</author>
         <link>https://padlet.com/manarmech/Bookmarks/wish/2058258261</link>
         <description><![CDATA[]]></description>
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         <pubDate>2022-02-21 07:29:00 UTC</pubDate>
         <guid>https://padlet.com/manarmech/Bookmarks/wish/2058258261</guid>
      </item>
      <item>
         <title></title>
         <author>manarmech</author>
         <link>https://padlet.com/manarmech/Bookmarks/wish/2058259361</link>
         <description><![CDATA[]]></description>
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         <pubDate>2022-02-21 07:29:42 UTC</pubDate>
         <guid>https://padlet.com/manarmech/Bookmarks/wish/2058259361</guid>
      </item>
      <item>
         <title></title>
         <author>manarmech</author>
         <link>https://padlet.com/manarmech/Bookmarks/wish/2058259993</link>
         <description><![CDATA[]]></description>
         <enclosure url="https://padlet-uploads.storage.googleapis.com/1559903212/4ad47dd6e7bef97505c6e0b9aaa87fba/image.png" />
         <pubDate>2022-02-21 07:30:09 UTC</pubDate>
         <guid>https://padlet.com/manarmech/Bookmarks/wish/2058259993</guid>
      </item>
      <item>
         <title></title>
         <author>manarmech</author>
         <link>https://padlet.com/manarmech/Bookmarks/wish/2058261066</link>
         <description><![CDATA[]]></description>
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         <pubDate>2022-02-21 07:30:54 UTC</pubDate>
         <guid>https://padlet.com/manarmech/Bookmarks/wish/2058261066</guid>
      </item>
      <item>
         <title></title>
         <author>manarmech</author>
         <link>https://padlet.com/manarmech/Bookmarks/wish/2058261790</link>
         <description><![CDATA[]]></description>
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         <pubDate>2022-02-21 07:31:22 UTC</pubDate>
         <guid>https://padlet.com/manarmech/Bookmarks/wish/2058261790</guid>
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      <item>
         <title></title>
         <author>manarmech</author>
         <link>https://padlet.com/manarmech/Bookmarks/wish/2058264233</link>
         <description><![CDATA[]]></description>
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         <pubDate>2022-02-21 07:33:00 UTC</pubDate>
         <guid>https://padlet.com/manarmech/Bookmarks/wish/2058264233</guid>
      </item>
      <item>
         <title></title>
         <author>manarmech</author>
         <link>https://padlet.com/manarmech/Bookmarks/wish/2058266054</link>
         <description><![CDATA[]]></description>
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         <pubDate>2022-02-21 07:34:15 UTC</pubDate>
         <guid>https://padlet.com/manarmech/Bookmarks/wish/2058266054</guid>
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      <item>
         <title></title>
         <author>manarmech</author>
         <link>https://padlet.com/manarmech/Bookmarks/wish/2058266486</link>
         <description><![CDATA[]]></description>
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         <pubDate>2022-02-21 07:34:34 UTC</pubDate>
         <guid>https://padlet.com/manarmech/Bookmarks/wish/2058266486</guid>
      </item>
      <item>
         <title></title>
         <author>manarmech</author>
         <link>https://padlet.com/manarmech/Bookmarks/wish/2058267344</link>
         <description><![CDATA[]]></description>
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         <pubDate>2022-02-21 07:35:11 UTC</pubDate>
         <guid>https://padlet.com/manarmech/Bookmarks/wish/2058267344</guid>
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      <item>
         <title></title>
         <author>manarmech</author>
         <link>https://padlet.com/manarmech/Bookmarks/wish/2058267835</link>
         <description><![CDATA[]]></description>
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         <pubDate>2022-02-21 07:35:31 UTC</pubDate>
         <guid>https://padlet.com/manarmech/Bookmarks/wish/2058267835</guid>
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      <item>
         <title></title>
         <author>manarmech</author>
         <link>https://padlet.com/manarmech/Bookmarks/wish/2058268291</link>
         <description><![CDATA[]]></description>
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         <pubDate>2022-02-21 07:35:49 UTC</pubDate>
         <guid>https://padlet.com/manarmech/Bookmarks/wish/2058268291</guid>
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      <item>
         <title></title>
         <author>manarmech</author>
         <link>https://padlet.com/manarmech/Bookmarks/wish/2058270375</link>
         <description><![CDATA[]]></description>
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         <pubDate>2022-02-21 07:37:06 UTC</pubDate>
         <guid>https://padlet.com/manarmech/Bookmarks/wish/2058270375</guid>
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      <item>
         <title>exocrine function </title>
         <author>manarmech</author>
         <link>https://padlet.com/manarmech/Bookmarks/wish/2058327332</link>
         <description><![CDATA[<div>Exocrine function</div><ul><li>Pancreatic acinar cells: responsible for production of digestive enzymes<ul><li>Amylase, lipase, colipase, phospholipase and proteases (trypsinogen + chymotrypsinogen)</li><li>These enzymes are stored within the acinar cell in secretory granules and are released by exocytosis</li></ul></li><li>After a meal, pancreatic exocrine secretion is regulated by cephalic, gastric and intestinal stimuli</li></ul><div><br></div><div>Cholecystokinin</div><ul><li>Produced in I cells (= specialised gut endocrine cells) of the mucosa of the small intestine</li><li>Secreted in response to intraluminal food</li><li>CCk acts via receptors on vagal afferent fibres to stimulate pancreatic secretion</li><li>Proteases and colipase are secreted as inactive precursors and require duodenal enterokinase to initiate activity</li><li>Secretin:&nbsp;</li></ul><div><br>Pancreatic Polypeptide</div><ul><li>Released from the islet cells from the pancreas in response to a meal&nbsp;</li><li>Has an inhibitory effect upon acinar enzyme secretion both by a local effect and via central receptors</li><li>Somatostatin:<br><br></li></ul><div><br></div><div><br></div><div><br></div>]]></description>
         <enclosure url="" />
         <pubDate>2022-02-21 08:16:07 UTC</pubDate>
         <guid>https://padlet.com/manarmech/Bookmarks/wish/2058327332</guid>
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      <item>
         <title>endocrine function </title>
         <author>manarmech</author>
         <link>https://padlet.com/manarmech/Bookmarks/wish/2058329229</link>
         <description><![CDATA[<ul><li>Consists of hormone-producing cells arranged in nests of islets (islets of Lagnerhans)</li><li>The hormones produces are secreted directly into the circulation and there is and access to the pancreatic ductular system</li><li>Five main types of islet cell corresponding to different secretory components:</li></ul><ol><li>Beta cell: most common, responsible for insulin production</li><li>Alpha cell: produces glucagon</li><li>D cell: produce somatostatin</li><li>PP cell: produce pancreatic polypeptide&nbsp;</li><li>Enterochromaffin cell: produce serotonin</li></ol><ul><li>Other hormones: gastrin-releasing peptide, neuropeptide Y and galanin → neurotransmitters active in the neuro-gastrointestinal axis<br><br></li></ul><div><br></div>]]></description>
         <enclosure url="" />
         <pubDate>2022-02-21 08:17:25 UTC</pubDate>
         <guid>https://padlet.com/manarmech/Bookmarks/wish/2058329229</guid>
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      <item>
         <title>classification</title>
         <author>manarmech</author>
         <link>https://padlet.com/manarmech/Bookmarks/wish/2058331209</link>
         <description><![CDATA[<div>Classification of pancreatitis</div><ol><li>Acute pancreatitis: process that occurs on the background of a previously normal pancreas and can return to normal after resolution of the episode</li><li>Chronic pancreatitis: continuing inflammation with irreversible structural changes</li></ol><ul><li>Differentiation between the two can be difficult.&nbsp;</li><li>Any of the causes of acute pancreatitis if untreated may result in recurrent episodes classified as acute relapsing pancreatitis</li><li>In other cases the recurrent episodes of recurrent pancreatitis may represent exacerbations of an underlying chronic process<br><br></li></ul><div><br></div>]]></description>
         <enclosure url="" />
         <pubDate>2022-02-21 08:18:48 UTC</pubDate>
         <guid>https://padlet.com/manarmech/Bookmarks/wish/2058331209</guid>
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      <item>
         <title>Basic characteristics and effect pancreas </title>
         <author>manarmech</author>
         <link>https://padlet.com/manarmech/Bookmarks/wish/2058334735</link>
         <description><![CDATA[<div>autosomal recessive disorder<br>CFTR gene --&gt; mutated&nbsp;<br>affects the cells that produce mucus, sweat and digestive juices.<br>--&gt; secretions to become sticky and thick. Instead of acting as lubricants, the secretions plug up tubes, ducts and passageways, especially in the lungs and pancreas.</div>]]></description>
         <enclosure url="" />
         <pubDate>2022-02-21 08:20:59 UTC</pubDate>
         <guid>https://padlet.com/manarmech/Bookmarks/wish/2058334735</guid>
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      <item>
         <title></title>
         <author>manarmech</author>
         <link>https://padlet.com/manarmech/Bookmarks/wish/2058341179</link>
         <description><![CDATA[]]></description>
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         <pubDate>2022-02-21 08:25:05 UTC</pubDate>
         <guid>https://padlet.com/manarmech/Bookmarks/wish/2058341179</guid>
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      <item>
         <title></title>
         <author>manarmech</author>
         <link>https://padlet.com/manarmech/Bookmarks/wish/2058350392</link>
         <description><![CDATA[]]></description>
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         <pubDate>2022-02-21 08:31:08 UTC</pubDate>
         <guid>https://padlet.com/manarmech/Bookmarks/wish/2058350392</guid>
      </item>
      <item>
         <title></title>
         <author>manarmech</author>
         <link>https://padlet.com/manarmech/Bookmarks/wish/2058372985</link>
         <description><![CDATA[]]></description>
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         <pubDate>2022-02-21 08:46:27 UTC</pubDate>
         <guid>https://padlet.com/manarmech/Bookmarks/wish/2058372985</guid>
      </item>
      <item>
         <title></title>
         <author>manarmech</author>
         <link>https://padlet.com/manarmech/Bookmarks/wish/2058391015</link>
         <description><![CDATA[<div><strong>Incidence</strong></div><ul><li>10 cases per 100000</li><li>the fifth most common cause of cancer death in the west</li><li>incidence increases with age &gt;60</li><li>&nbsp;60% of patients with this condition are male.&nbsp; adenocarcinoma in type and the large majority are of ductal origin.</li></ul><div><strong>Aetiology&nbsp;</strong></div><ul><li>risk factors : Smoking is associated with a two-fold increase. Excess intake of alcohol, intake of coffee and use of aspirin, history of diabetes and chronic pancreatitis, 5–10% of patients with pancreatic cancer have a family history of the disease</li></ul><div><strong>Clinical picture</strong></div><ul><li>Head of pancreas and the ampulla of Vater.&nbsp;<ul><li>most frequent site for cancer to develop.</li><li>present earlier with obstruction to the bile duct as this passes through the head of pancreas giving jaundice&nbsp;<br>localised lesions painless → pain: tumour progression.&nbsp;</li><li>Obstruction of the pancreatic duct → symptomatic episodes of pancreatitis.</li><li>Pancreatic damage secondary to duct obstruction is frequently associated with abnormalities of glucose homeostasis.&nbsp;</li><li>jaundice with characteristic scratch marks secondary to cholestasis.&nbsp;</li><li>Sometimes the gallbladder will be palpable (Courvoisier’s sign).&nbsp;</li><li>With metastatic disease, a central abdominal mass may be palpable as well as hepatomegaly.</li></ul></li><li>Carcinoma localised to the body or tail of the pancreas<ul><li>&nbsp;abdominal pain, anorexia and weight loss</li><li>Pain is often dull in character with radiation through/into the back</li><li>partial relief of pain by sitting forward.&nbsp;</li><li>Bile duct obstruction and jaundice is&nbsp; late phenomena</li></ul></li></ul><div><strong>investigations</strong></div><ul><li>Transabdominal ultrasound</li><li>Contrast-enhanced CT scan&nbsp;</li><li>Laparoscopy</li><li>ERCP(Endoscopic retrograde cholangiopancreatography)<em>&nbsp;</em></li><li>Percutaneous needle biopsy&nbsp;</li><li>MRI scanning and endoscopic ultrasound&nbsp;</li><li>Several tumour markers<em>&nbsp;</em></li></ul><div><strong>differential diagnosis</strong></div><ul><li>IgG4-related autoimmune pancreatitis</li></ul><div><strong>management&nbsp;</strong></div><ul><li><strong>Endoscopic placement of endoprostheses </strong>(stents)&nbsp;</li><li><strong>&nbsp;Palliative surgery </strong>&nbsp;in duodenal obstruction&nbsp;</li><li><strong>&nbsp;Radiotherapy</strong> results have been disappointing&nbsp;</li><li><strong>Chemotherapeutic agents</strong></li></ul>]]></description>
         <enclosure url="" />
         <pubDate>2022-02-21 09:00:08 UTC</pubDate>
         <guid>https://padlet.com/manarmech/Bookmarks/wish/2058391015</guid>
      </item>
      <item>
         <title></title>
         <author>manarmech</author>
         <link>https://padlet.com/manarmech/Bookmarks/wish/2058391237</link>
         <description><![CDATA[]]></description>
         <enclosure url="https://padlet-uploads.storage.googleapis.com/1559903212/955aca4b48fa1d3f338f02c4c9e7e370/image.png" />
         <pubDate>2022-02-21 09:00:19 UTC</pubDate>
         <guid>https://padlet.com/manarmech/Bookmarks/wish/2058391237</guid>
      </item>
      <item>
         <title></title>
         <author>manarmech</author>
         <link>https://padlet.com/manarmech/Bookmarks/wish/2058392096</link>
         <description><![CDATA[]]></description>
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         <pubDate>2022-02-21 09:01:03 UTC</pubDate>
         <guid>https://padlet.com/manarmech/Bookmarks/wish/2058392096</guid>
      </item>
      <item>
         <title></title>
         <author>manarmech</author>
         <link>https://padlet.com/manarmech/Bookmarks/wish/2058402224</link>
         <description><![CDATA[<div>Bilirubin metabolism</div><ul><li>1. Bilirubin is produced from breakdown of mature red cells by Kupffer cells in the liver and reticuloendothelial system; 15% of bilirubin is formed from catabolism of other haemcontaining proteins<ul><li><ul><li>Normally, 250–300 mg daily. </li></ul></li></ul></li><li>2.  unconjugated bilirubin is water-insoluble, due to internal hydrogen bonding, and is transported to the liver attached to albumin.&nbsp;</li><li>3. Bilirubin dissociates from albumin and is taken up by hepatic cell membranes and transported to the endoplasmic reticulum by cytoplasmic proteins, where it is conjugated with glucuronic acid and excreted into bile.&nbsp;</li><li>4.. conjugated bilirubin is water-soluble and is actively secreted into biliary canaliculi and excreted into the intestine within bile&nbsp;</li><li>5. not absorbed from the small intestine because of its large molecular size</li><li>6. In the terminal ileum, bacterial enzymes hydrolyse the molecule, releasing free bilirubin which is then reduced to urobilinogen, some of which is excreted in the stools as stercobilinogen. The remainder is absorbed by the terminal ileum, passes to the liver via the enterohepatic circulation, and is re-excreted into bile. Then excreted kidneys<ul><li>= When hepatic excretion of conjugated bilirubin is impaired, a small amount is strongly bound to serum albumin and is not excreted by the kidneys; it accounts for the persistent hyperbilirubinemia</li></ul></li></ul><div><br></div>]]></description>
         <enclosure url="" />
         <pubDate>2022-02-21 09:09:00 UTC</pubDate>
         <guid>https://padlet.com/manarmech/Bookmarks/wish/2058402224</guid>
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      <item>
         <title>Jaundice</title>
         <author></author>
         <link>https://padlet.com/manarmech/Bookmarks/wish/2058403572</link>
         <description><![CDATA[<div><a href="https://www.msdmanuals.com/professional/hepatic-and-biliary-disorders/approach-to-the-patient-with-liver-disease/jaundice">https://www.msdmanuals.com/professional/hepatic-and-biliary-disorders/approach-to-the-patient-with-liver-disease/jaundice</a></div>]]></description>
         <enclosure url="https://www.msdmanuals.com/professional/hepatic-and-biliary-disorders/approach-to-the-patient-with-liver-disease/jaundice" />
         <pubDate>2022-02-21 09:09:55 UTC</pubDate>
         <guid>https://padlet.com/manarmech/Bookmarks/wish/2058403572</guid>
      </item>
      <item>
         <title></title>
         <author>manarmech</author>
         <link>https://padlet.com/manarmech/Bookmarks/wish/2058408898</link>
         <description><![CDATA[]]></description>
         <enclosure url="https://padlet-uploads.storage.googleapis.com/1559903212/4cbabf7f485bc192cda56a0f5e06603a/image.png" />
         <pubDate>2022-02-21 09:13:44 UTC</pubDate>
         <guid>https://padlet.com/manarmech/Bookmarks/wish/2058408898</guid>
      </item>
      <item>
         <title></title>
         <author>manarmech</author>
         <link>https://padlet.com/manarmech/Bookmarks/wish/2058410901</link>
         <description><![CDATA[]]></description>
         <enclosure url="https://padlet-uploads.storage.googleapis.com/1559903212/d463228e7a60ec1692131f9e319cb02f/image.png" />
         <pubDate>2022-02-21 09:15:08 UTC</pubDate>
         <guid>https://padlet.com/manarmech/Bookmarks/wish/2058410901</guid>
      </item>
      <item>
         <title>Cullens Sign and Grey Turners Sign</title>
         <author>mmtzclaros1</author>
         <link>https://padlet.com/manarmech/Bookmarks/wish/2058628624</link>
         <description><![CDATA[]]></description>
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         <pubDate>2022-02-21 11:52:26 UTC</pubDate>
         <guid>https://padlet.com/manarmech/Bookmarks/wish/2058628624</guid>
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