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Pancreas by Clarisse my


Clarissa Roberto-Lucero ,M.D. Gastrointestinal fellow UP-PGH

• 12-15 cm long, 70 –110g • lies w/in the curvature of the duodenum;body and tail lies in the posterior abdomen and the latter extends to the spleen • blood supply is mainly from celiac and superior mesenteric artery • celiac  gastroduodenal artery  anterior and posterior superior pancreaticoduodenal artery • superior mesenteric artery  ant and post inferior pancreaticoduodenal arteries

• Venous drainage flows into the portal systems • lymphatics terminate in pancreaticosplenic pancreaticoduodenal and preaortic LN • innervation is thru vagal and splanchnic nerves

• Finely nodular gland,surrounded by fine ct,without definite fibrous capsule • 80% exocrine and 2% endocrine • The lumen of acinus is the origin of secretory duct and contains centroacinar cells * unique to pancreas • Main cell types are acinar,ductal and islet cells • Lumen of acinus   intralobular ducts  interlobular ducts  main pancreatic duct

• acinar cells are tall pyramidal or columnar EC, resting state- zymogen granules fills the apical part and basal part has 1-2 nuclei, endoplasmic reticulum containing ribosomes and golgi apparatus feeding statezymogen granules sre depleted, golgi complex located in the apex • Islet of Langerhans consist of anastomosing • Cords of polygonal endocrine cells: B cells 50-80%, A cells 5-20%, PP 10-35 %,D cells 5 %

Functional Anatomy
• The functional unit of exocrine pancreas is composed of acinus and draining ductule • Acinus is specialized to synthesize, store and secrete digestive enzymes • basolateral has the receptors for hormone and Ntransmitters; Basal has the nucleus and ER; Apical region contains the zymogen granules

Composition of the Exocrine Pancreatic Secretions
• Inorganic components: water,Na K Cl HCO3 • Pancreatic juice : 0.2-0.3 ml/min in resting state to 4ml/min during stimulation • Major stimulus for exocrine secretion is SECRETIN via camp pathway • Organic constituents: major proteolytic,amylolytic,lipolytic,nuclease digestive enzymes • Secreted in INACTIVE form and also secreted is the trypsin inhibitor

• Secreted by pancreas and salivary gland,both with identical enzyme activity, they differ in MW,CHO content and electrophoretic activity • Digest starch and glycogen • Hydrolyze 1,4-glycoside linkages • Amylase activity in the stomach is protected from gastric acid by buffering of meal and alkaline environment of saliva and gastric mucous

• Pancreas secretes 3 lipase; Lipase,phospholipase A2 and carboxylesterase • The most important source is the pancreas • Needs bile acid and colipse for full activity • Hydrolyzes TAG to 2 FA and 1 monoglyceride • Phospholipase A2 hydrolyzes FA at position 2 in Phosphatidylcholine • carboxylesterase cleaves cholesterol esters,lipidsoluble vitamin esters,triglycerides,diglycerides and monoglycerides; Bile salts are also needed

Acute Pancreatitis
• Severe pain in the upper abdomen • Amylase and lipase are increased at least 3x • Severe pancreatitis may cause ductal obstruction • Patient may developed DM and steatorrhea • Contrast enhanced CT distinguish interstitial from necrotizing pancreatitis

Acute Pancreatitis
• MILD : minimal or no organ dysfxn and uneventful recovery • SEVERE : organ failure,(+) abscess/necrosis/pseudocyst,  3 Ranson’s or  8 APACHE II points • Organ failure: shock – SBP < 90mmhg pao2 60mmhg, creatinine >2mg/dl and GI bleeding > 500ml/24h

Acute Pancreatitis
• Acute fluid collection- less than 3cm,low attenuation,occurs 30-50% and resolved spontaneously • Pseudocyst : 4-6 weeks ,encapsulated • Pancreatic necrosis

Acute Pancreatitis
• Pancreatic abscess: usually developed 4 weeks after the onset of acute pancreatitis mortality is less than in infected necrosis • Terms deleted are phlegmon,infected pseudocyst, hemorrhagic pancreatitis and persistent acute pancreatitis

Acute Pancreatitis Pathology
• Most common causes are : alcohol,gallstone and drugs • Interstitial pancreatitis: edema and inflammatory infiltrates ,no necrosis and hemorrhage • Necrotizing pancreatitis: macroscopic necrosis,fat necrosis occasionally hemorrhage

Acute Pancreatitis Pathogenesis
• Activation of trypsinogen to trypsin • TAP concentration correlates with severity of pancreatic inflammatory response,with highest levels with acinar necrosis and pancreatic hemorrhage • Protective mechanism : enzyme in inactive form, sequestered w/in compartment, protease inhibitors and enzyme are separated from lysosomal hydrolases as they pass the Golgi complex

Acute Pancreatitis Pathogenesis
• Common channel theory: gallstone impacted in the papilla causes reflux of bile from CBD into the pancreatic duct • Incompetence of sphincter of Oddi • Impaction of gallstone in the CBD raising intraductal pancreatic pressure damaging the ductal and acinar cells

Acute Pancreatitis Pathophysiology
• Activation of pancreatic enzymes • autodigestion of parenchyma • Absorption of activated enzyme into systemic circulation • ARDS: O2 free radicals ,leukocyte phospholipase A2 , PAF and TNF • Role of pancreatic microcirculation

Predisposing Conditions
• Gallstones : 30-75% • Idiopathic pancreatitis are caused by microlithiasis • Alcohol : 30% ; relaxation of sphincter of Oddi; Toxic-metabolic hypothesis • hyperlipidemia :4% • Hereditary pancreatitis : at least 2 family members • hyperparathyroidism and hypercalcemia • Structural abnormality in the ampullary region

Predisposing Conditions
• Sphincter of Oddi dysfuction • Obstruction of main pancreatic duct • Dehydration,hypovolemia, hypotension may lead to pancreatic ischemia • Infection: Coxsakie,EBV,hepatitis A/B/C,MMR ,TB,leptospirosis,brucellosis,Candida, C. sinensis and ascaris • Ergotamine overdose,arterial embolization for HCC and atheromatous embolization to pancreas

Predisposing Conditions
• ERCP induced :5%; Contributing factors are volume and pressure of contrast media injected, number of injection to pancreatic duct, ampullary trauma, overfilling of pancreatic duct,bacteria,sphincterotomy and insertion of stents and prior history of acute pancreatitis

Pancreatic Trauma
• • • • Penetrating or blunt trauma In penetrating trauma: laparotomy is essential In blunt trauma: is the pancreas injured Serum amylase activity may be increased whether or not the pancreas is injured • CT scan: show enlargement,contusion,subcapsular hematoma or E/N w/in 2 days despite presence of pancreatic trauma • ERCP- assess pancreatic ductal injury

Clinical Manifestation
• Abdominal pain : upper abdomen,rarely LLQ,moderate to severe,reaches max intensity w/in 10-20mins,,unbearable • Nausea and vomiting • Mild pancreatitis : may not appear ill • Pancreatic encephalopathy • Systemic toxicity,third spacing unstable vital signs • Evidence of jaundice and pleural effusion, abdominal distension, tenderness rarely rigid,Grey turner sign,Cullens sign and SQ fat necrosis

Laboratory Diagnosis
• Amylase: 40-45% from pancreas and 55-60% from salivary gland • Elevated in 75% of patients w/ AP from day1 to day5-10 of illness • Not elevated in patients with chronic pancreatitis ,hypertriglyceridemia and late measurement

Laboratory Diagnosis
• Lipase :elevated on the first day and remain elevated for longer period • More specific • Elevated in patients with renal insufficiency Crea Cl less than 20ml/min and in patients with inflamed or perforated intestines • Non pancreatitis elevation are less than twice the normal

Miscellaneous Test
• immunoreactive trrypsinogen,elastase,ribonuclease, phospholipase A2 • No advantage over amylase and lipase • PAP and PSP as accurate as amylase and may help in establishing prognosis • ALT greater than 150 IU/L is specific for gallstone pancreatitis in 96%

Test That Reflect Severity of Pancreatic Injury
• • • • • • • Hematocrit less than 50% WBC count > 16,000 Increased BUN Metabolic acidosis Low O2 saturation Decreased Ca Anatomic derangement : UTZ.CT scan ERCP

Radiologic Features
• Extension of pancreatic exudate into pararenal space and lesser sac • Anterior displacement of stomach • Sentinel loop • Ileus ( cecum,duodenum,ileum) • Colon cut off sign • Calcified gallstone,pancreatic stones • Ascites • CXR : atelectasis,pleural effusions,evidence of CHF and ARDS

CT Scan
3 main indications • 1. To r/o mesenteric infarction and Perforations • 2. Staging the severity • 3. Define presence of complications

CT Grading System of Balthazar and Ranson
• GradeA normal appearing pancreas • Grade B focal/diffuse enlargement • Grade C mild peripancreatic inflammatory changes • Grade D fluid collection in a single collection • GradeE 2 or more fluid collections near the pancreas or gas within the pancreas or peripancreatic inflammation

Differential Diagnosis
• • • • • • • Biliary colic Perforated hollow viscus Mesenteric ischemia Intestinal obstruction Inferior wall MI Dissecting aneurysm ectopic pregnancy

Ranson’s Criteria
• On admission: Age >55 WBC > 16,000/mm3 Glucose > 200mg/dl LDH >350 IU/l AST > 250 IU/l

Ranson’s Criteria
• During initial 48 hours Hematocrit decrease of >10mg/dl BUN increase of >5mg/dl Ca < 8mg/dl Pao2 < 60 mmHg Base deficits >4 meq/l Fluid sequestration >6L

Early Prognostic Signs
• Ranson’s : 5/11 measured at the time of admission Reflects the intensity and local inflammation

Early Prognostic Signs
 6/11 measured within the initial 48 hours reflects the systemic complication and effect of third space loss • Ranson’s score was 1.6 in mild , 2.4 in severe and 5.6 in lethal pancreatitis

Acute Pancreatitis
• Ranson’s score of more than 6 had higher incidence of complication,necrosis and infection • Overall sensitivity 57-85% and specificity of 68-85%

Early Prognostic Signs
APACHE II assess the degree of abnormality of 12 physiologic variables, age,and chronic health status Score of  9 within 48h have survived,whereas scores of  13 have likelihood of mortality Lack sensitivity and appears no better than other scoring system

Other Markers
• Amylase does not distinguish mild from severe pancreatitis • CRP is higher in severe and necrotizing pancreatitis; Activity peaks 36-48h • IL6 peak activity is between 24-36 h • PMN leukocyte elastase higher in severe and necrotizing pancreatitis, with high sensitivity and specificity • TAP in urine also assess severity after 48h of symptom

Other Prognostic Sign
• Obese patients have higher incidence of respiratory failure and severe pancreatitis • Obesity is an early prognostic sign • Presence of pleural effusion within 72h on CT scan, to 6 days on CXR correlate with more severe disease • Organ failure and local complications correlate with poor prognostic disease

Goals of Treatment
• Supportive treatment : fluid resuscitation,pulmonary care, ICU care • Limit systemic complication • Prevent pancreatic necrosis • Prevent pancreatic infection

Limitation of Systemic Complication
• Reduction in pancreatic secretion: Aprotinin • Inhibition of circulating inflammatory mediator and peritoneal lavage: ineffective in reducing morbidity and mortality • ERCP to remove gallstone in CBD: this eliminated sepsis but didn’t reduce mortality

Medical Management of Mild Pancreatitis
• • • • Adequte fluid resuscitation Pain reliever NGT insertion Refeeding

Medical Management of Severe Pancreatitis
• Fluid resuscitation may require > 5-6 l/day and at times more than 10L • Use of colloids if albumin is less than 2g/l • If Hct < 25 %- PRBC tansfusion • ARDS is the most serious respiratory complication, occuring on the 2nd to the 7th day, associated with dyspnea and progressive hypoxemia • Cardiovascular care, relief of pain, treatment of infection,metabolic complication and nutritional support

• Pancreatic necrosis  systemic toxicity and organ failure • Infected necrosis  guided percutaneous aspiration surgical debriment • Pancreatic pseudocyst : 5cm for 6weeks should be decompressed surgically to prevent bleeding,perforation and infection • Pseudocyst can be treated surgically, endoscopically and radiologically • Pancreatic abscess can be treated with percutaneous catheter drainage

• Pseudocyst can be treated surgically, endoscopically and radiologically • Pancreatic abscess can be treated with percutaneous catheter drainage

Systemic Complications
• • • • • • • Respiratory Cardiovascular Renal CNS SQ fat necrosis and bone abnormalities GI bleeding Splenic hematoma

• Mortality with interstitial AP is close to 0% • Mortality with Necrotizing AP is 10% • Alcoholic and gallstone pancreatitis have equally low mortality • Higher mortality is associated with idiopathic and postoperative pancreatitis

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