Pancreas Review. I am made in K cells and travel to the pancreass after meals to increase insulin release. GIP I target the biliopancreatic system after meals and increase pancreatic bicarb secretion and also the delivy of bile. CCK
I am made in K cells and travel to the pancreass after meals to increase insulin release.
I target the biliopancreatic system after meals and increase pancreatic bicarb secretion and also the delivy of bile.
I am mostly produced in the pancreas, and target the liver to increase glycogenolysis and gluconeogenesis. I am inhibited by somatostatin. I also go to fat and increase lipolysis and ketogenesis.
Similar to CCK, I increase panc and bile secretion. I can be used to help diagnose hypergastrinemia.
Stimulated by presence of CCK, I inhibit pancreatic secretion, and GB contraction, and slow down the foregut in the post-prandial state
Bonus: How is PPP used clinically?
Tumor marker for APUDoma’s
Stimulated by intraluminal fat, I also slow down the foregut in the post-prandial state
What is the name of the main pancreatic duct to increase insulin release.
The Duct of Wirsung
Mindless fact: Wirsung was murdered in Padua in 1643 over a fight about who really discovered the duct. Dr. Bartholin was also a co-discoverer.
What is the name of the small pancreatic duct
Duct of Santorini
Santorini was a Venetian anatomist and his star pupil was Vater. What did Vater name?
Where is the Supreme Artery of Kirk
Dorsal Pancreatic artery
Which pancreatic bud is connected to the bile duct to increase insulin release.
Which bud migrates posteriorly and left to fuse with the other
Ventral migrates towards dorsal
Which duct comes from the ventral bud
What does the ventral bud become
Uncinate and inferior head
The dorsal bud has the duct of wirsung and makes up the sup. Head, body, and tail
Which bud abnomally fuses and causes an annular pancreas? to increase insulin release.
The ventral bud migrates ant and post but fails to fuse
How does it present and what is common pre-existing co-morbidity
Bowel obstruction in newborn period , Down’s syndrome.
What is the treatment
What condition is caused by failure of ducts to fuse
Who do you treat and what is treatment
Recurrent attacks, ERCP/sphincterotomy/papillotomy, lap chole.
Which common meds are associated with pancreatitis to increase insulin release.
Proven: Azathioprine, Lasix, depakote, thiazides, tetracycline, sulfonamide, H2 blockers
Suspected: steroids, Tacrolimus, flagyl, 6-mp
What metabolic causes can cause pancreatitis
Hypertriglycidemia, and hypercalcemia
What surgical diseases may cause pancreatitis
Perforated peptic ulcer, crohn’s of duodenum
Which enzymes are responsible for to increase insulin release.
Pancreatic necrosis (in the presence of bile)
Bonus: How does PLA2 affect lungs during pancreatitis
By digesting pulmonary surfactant and causing ARDS
What signs are seen on a flat-plate for acute pancreatitis to increase insulin release.
Sentinel loops, colon cut-off, dilated duodenum
What is a sentinel loop
Adynamic dilated loop of SB with small focal area of inflammation related to panc. Associated ileus.
What signs are seen on a flat-plate for chronic pancreatitis
Dilated panc. Duct, calcifications, parenchymal atrophy
Chain of lakes
What are the early ranson’s criteria to increase insulin release.
What are the late criteria?
HCT drop >10
+ fluid sequ by 4L
BUN up by 5 from baseline
Which of the following are indications for necrosectomy? to increase insulin release.
>50% pancreatic necrosis by CT
Bile duct stricture
Refractory Shock for >3 days
What % of people with GB pancreatitis will recur within 8 weeks if GB not removed
What are the absolute indications for surgery in chronic pancreatitis?
Refractory disabling pain
GI or biliary obstruction
Recurrent acute exacerbations
Splenic V thrombosis with portal HTN
What % of patients with chronic pancreatitis will get a pseudocyst?
What % of patients with acute pancreatitis will get a persistant pseudocyst?
What is most common cause for children to get pseudocyst
What % of periampullary tumors come from: pseudocyst?
What tumor marker is the most useful
CA 19-9 has the highest sens and spec.
BRCA 2, HNPCC, Peutz-Jeghers, MEN1, p-53
What is the most common benign neoplasm in the pancreas
What is the most common cystic lesion in the pancreas
Courvoisier lived in Switzerland in 1880’s and fought in Franco-Prussian (7-years war). Did internships with Lister and Bilroth
What rash do patients with glucagonoma get pseudocyst?
Nec Mig Ery. Also anemia, glossitis, and weight loss (rem: all malignant)
What do patients with VIPomas get
WDHA (rem: 50% malignant)
What do patients with somatistatinomas get
Gallstones, DM, and steatorrhea (rem: all malignant)
What will the question mention in gastrinoma?
H. Pylori negative. (1/2 malig), never malign when in MEN 1 (10% of time)
Bonus: 2nd most common location of gastrinoma following pancreas
Duodenum. (submucosal) in triangle
Who am I? pseudocyst?
Sunburst pattern on CT, rarely malignant
Serous cystadenoma ( Sunny and not Serious)
I am frequently malignant and have peripheral calcifications
Mucinous (M Malig)
I am premalignant and require excision with clear margins “fishmouth” duct with mucus pathogen.