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43 Cards in this Set
- Front
- Back
Embryologic development of the pancreas
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dorsal and ventral buds -> ventral swings around to join the dorsal bud -> they fuse and the duct of santorini (of the dorsal bud) usually fuses with them main duct of Wirsong
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Blood supply of the pancreas
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head and uncinate: gastroduodenal and superior mesenteric arteries ; body and tail: splenic artery
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Action of secretin
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produced by duodenum in response to fatty acids -> stimulates water and bicarbonate secretion by the pancreas
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Action of cholecystokinin
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produced by duodenum -> stimulates secretion of digestive proenzymes by the pancreas
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Pancreatic enzymes produced in active form
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don't need trypsin: amylase and lipase
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Action of VIP
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induces glycogenolysis and hyperglycemia, stimulates GI fluid secretion
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Annular pancreas
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malrotation of the ventral bud of the pancreas that can lead to duodenal obstruction
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Pancreas divisum
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5-7 % of pop has no fusion of duct of wirsong and santorini, the bulk of the pancreas exits via the duct of santorini and the minor papilla, often get obstruction and recurrent pancreatitis
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Complication of atypically shaped/distributed pancreas
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asymptomatic unless accidentally taken out in surgery from not expecting it to be there
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Most common causes of acute and chronic pancreatitis
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acoholism and biliary tract obstruction
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Morphology of acute pancreatitis
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edema from microvascular leakage, fat necrosis from release of lipolytic enzymes that possibly spreads to other structures, typically no involvment of inflammatory cells, proteolytic digestion of pancreatic parenchyma, usually reversible
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Clinical manifestation of acute pancreatitis
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sudden, epigastric pain radiating to the back, elevation of serum amylase and lipase, can devleop into shock, renal fialure, acute respiratory fialure and sepsis, dehydration; Grey-Turner sign: bruising of the flank, Cullen's sign: periumbilical bruising, elevated serum amylase and lipase
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Complications of acute pancreatitis
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pseudocyst formation, pancreatic absces, peritonitis, pancreatic ascities, involvement of adjacent organs, obstructive jaundcie, fetal loss
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Pathophysiology of multi-organ failure from acute pancreatitis
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intense release of cytokines and pancreatic enzymes into the blood -> diffuse damage to tissues, much more common with pancreatic necrosis
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Treatment of acute pancreatitis
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rehydration and gut rest, supportive care, antibiotics (especially imipenem)
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Indications for early ERCP in acute pancreatitis
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pregnant or severe pancreatis from gall stone
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Pathophysiology of chronic pancreatitis
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repeated bouts of acute pancreatitis -> atrophy and destruction of acini -> fibrosis -> last to be damaged is beta cells of the islet of langerhans, ducts dilate
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How is acute different from chronic pancreatitis
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chronic has irreverisible impairment of pancreatic function
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Causes of chronic pancreatits
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alcoholism, obstruction, hyperparathyroidism, hyperlipidemia, pancreas divisum, hereditary pancreatitis, mutatoin in CFTR (different polymorphism from cystic fibrosis
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Mechanism for alcohol induced pancreatitis
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alcohol increases protein concentratoin in pancreatic juice -> forms concretions in the ducts -> ducts obstructed ; oxidative stress, direct toxic affect on acinar cells
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Clinical presentation of chronic pancreatitis
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may have repeated attacks with jaundice, may have vague attacks of indigestion, may be relatively silent until late stage DM develops
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Complications of chronic pancreatitis
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pancreatic maldigestion, pancreatic diabetes, pleural or pericardial effusion, pancreatic ascites, portal hypertension, ischemic necrosis of bone (from hemoconcentration), addiction to narcotics (from chronic hard to manage pain) retinopathy, carcinoma
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Pancreatic pseudocyst
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walling off of areas of hemorrhagic fat necrosis by fibrous tissue without an epithelial lining (pseudocyst)
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use of CT with pancreatitis
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important for diagnosis and for prognosis of pt, detects severe pancreatitis, lack of enhancement with contrast shows necrosis of the pancreas
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Lab values for gallstone pancreatitis
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ALT > 150
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Some causes of pancreatitis that should be diagnsoed with ERCP
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microlithiasis, sphincter of oddi dysfunction, pancreas divisum
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Indications of severe acute pancreatitis
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hypotensive, hypoxic, GI bleed
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Ranson Scoring system
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scores severity of acute pancreatitis: scoring for age >55, WBC >16k, glucose >200, elevated LDH and AST, elevated hematocrit, BUN, calcium, PaOs, fluid sequestration ; if greater than 3 points is likely to be or develop into severe pancreatitis
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use of hematocrit in acute pancreatitis
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if Hct is >44 after 24 hrs of hydration predicts necrosis
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Common age of pancreatic carcinoma
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60-80
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Risk factors for pancratic carcinoma
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strongest is smoking, high fat diet, low physical activity, chronic pancreatitis, diabetes melitis, alchoholism, occupational epxosure to certain hydrocarbons; genetics syndromes: heridatry nonpolyposis colon cancer, hereditary breast and ovarian, peutz-jegher's, ataxia telangiectasia, familial atypcal multiple mole melanoma syndrome
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common cytogenetics of pancreatic carcinoma
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Kras mutation at codon 12 (80-90%)
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Precursor lesions to pancreatic carcinoma
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pancreatic intraepithelial neoplasias
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Most common sites of pancratic carcinomas
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head > dffuse > body > tail
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clinical presentation of pancreatic carcinomas
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involvement of head: early obstructive jaundice, may be painless, wieght loss (catch earlier); involvement of tail: insidious onset with weight loss and pain, Trousseau's sign (malignancy leading to coagulation), often present with distant metastasis
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Most common type of histologic pattern of pancreatic carcinoma
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ductal adenocarcinoma, grow all around the wall leading to functional obstruction, often see desmoplasia next to atrophic and fibrotic parenchyma; perineural, lymphatic and vascular invasion common and makes resection difficult; invasion in to adjacent structures and frequent metastasis
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Desmoplasia
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reactive fibrosis from malignancy, surrounds the malignancy
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presentatoin of neoplasms of the ampulla of vater and terminal common bile duct
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present early with jaundice so have better prognosis
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Prognosis of pancreatic endocrine tumor vs. pancreatic carcinoma
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worse with pancreatic carcinoma
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Treatment of pancreatic carcinoma
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whipple procedure: removed ampulla of the stomach, portion of duodenum and head of the pancreas, only performed if there are no lymph nodes positive for metastasis
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Some pancreatic endocrine tumors
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insulinoma, gastrinoma, VIPoma, glucagonoma
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Presentation of insulinoma
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whipple triad: attacks of hypoglycemia, anxiety cold sweat and confusion, attacks precipitated by fasting or exercise, relieved by ingesting sugar
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Presentation of VIPoma
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werner -morrison syndrome: severe watery diarrhea, hypokalemia, achlorhydria (low HCl in gut)
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