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43 Cards in this Set

  • Front
  • Back
Embryologic development of the pancreas
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
Blood supply of the pancreas
head and uncinate: gastroduodenal and superior mesenteric arteries ; body and tail: splenic artery
Action of secretin
produced by duodenum in response to fatty acids -> stimulates water and bicarbonate secretion by the pancreas
Action of cholecystokinin
produced by duodenum -> stimulates secretion of digestive proenzymes by the pancreas
Pancreatic enzymes produced in active form
don't need trypsin: amylase and lipase
Action of VIP
induces glycogenolysis and hyperglycemia, stimulates GI fluid secretion
Annular pancreas
malrotation of the ventral bud of the pancreas that can lead to duodenal obstruction
Pancreas divisum
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
Complication of atypically shaped/distributed pancreas
asymptomatic unless accidentally taken out in surgery from not expecting it to be there
Most common causes of acute and chronic pancreatitis
acoholism and biliary tract obstruction
Morphology of acute pancreatitis
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
Clinical manifestation of acute pancreatitis
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
Complications of acute pancreatitis
pseudocyst formation, pancreatic absces, peritonitis, pancreatic ascities, involvement of adjacent organs, obstructive jaundcie, fetal loss
Pathophysiology of multi-organ failure from acute pancreatitis
intense release of cytokines and pancreatic enzymes into the blood -> diffuse damage to tissues, much more common with pancreatic necrosis
Treatment of acute pancreatitis
rehydration and gut rest, supportive care, antibiotics (especially imipenem)
Indications for early ERCP in acute pancreatitis
pregnant or severe pancreatis from gall stone
Pathophysiology of chronic pancreatitis
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
How is acute different from chronic pancreatitis
chronic has irreverisible impairment of pancreatic function
Causes of chronic pancreatits
alcoholism, obstruction, hyperparathyroidism, hyperlipidemia, pancreas divisum, hereditary pancreatitis, mutatoin in CFTR (different polymorphism from cystic fibrosis
Mechanism for alcohol induced pancreatitis
alcohol increases protein concentratoin in pancreatic juice -> forms concretions in the ducts -> ducts obstructed ; oxidative stress, direct toxic affect on acinar cells
Clinical presentation of chronic pancreatitis
may have repeated attacks with jaundice, may have vague attacks of indigestion, may be relatively silent until late stage DM develops
Complications of chronic pancreatitis
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
Pancreatic pseudocyst
walling off of areas of hemorrhagic fat necrosis by fibrous tissue without an epithelial lining (pseudocyst)
use of CT with pancreatitis
important for diagnosis and for prognosis of pt, detects severe pancreatitis, lack of enhancement with contrast shows necrosis of the pancreas
Lab values for gallstone pancreatitis
ALT > 150
Some causes of pancreatitis that should be diagnsoed with ERCP
microlithiasis, sphincter of oddi dysfunction, pancreas divisum
Indications of severe acute pancreatitis
hypotensive, hypoxic, GI bleed
Ranson Scoring system
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
use of hematocrit in acute pancreatitis
if Hct is >44 after 24 hrs of hydration predicts necrosis
Common age of pancreatic carcinoma
60-80
Risk factors for pancratic carcinoma
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
common cytogenetics of pancreatic carcinoma
Kras mutation at codon 12 (80-90%)
Precursor lesions to pancreatic carcinoma
pancreatic intraepithelial neoplasias
Most common sites of pancratic carcinomas
head > dffuse > body > tail
clinical presentation of pancreatic carcinomas
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
Most common type of histologic pattern of pancreatic carcinoma
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
Desmoplasia
reactive fibrosis from malignancy, surrounds the malignancy
presentatoin of neoplasms of the ampulla of vater and terminal common bile duct
present early with jaundice so have better prognosis
Prognosis of pancreatic endocrine tumor vs. pancreatic carcinoma
worse with pancreatic carcinoma
Treatment of pancreatic carcinoma
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
Some pancreatic endocrine tumors
insulinoma, gastrinoma, VIPoma, glucagonoma
Presentation of insulinoma
whipple triad: attacks of hypoglycemia, anxiety cold sweat and confusion, attacks precipitated by fasting or exercise, relieved by ingesting sugar
Presentation of VIPoma
werner -morrison syndrome: severe watery diarrhea, hypokalemia, achlorhydria (low HCl in gut)