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PANCREAS
OBJECTIVES
โ€ข Understand the etiology/risk
factors, pathogenesis,
morphology, clinical features
and outcome of pancreatic
inflammations and
neoplasms
Ventral Bud
Chapter 19
Posterior view of duodenum/pancreas
Arterial supply and venous drainage of the
pancreas and spleen
Lymphatic drainage of the distal
pancreas and spleen
Hepaticopancreatic ampulla
(Ampulla of Vater)
L2
makes HCO3ยฏ
Pancreatic Enzymes
โ€ข
โ€ข
โ€ข
โ€ข
โ€ข

Amylase
Lipase
DNA-ase
RNA-ase
Zymogens: Trypsinogen
Chymotrypsinogen
Procarboxypeptidase A, B
PANCREAS DISEASES
โ€ข Congenital

โ€ข Inflammatory
โ€“Acute
โ€“Chronic

โ€ข Cysts

โ€ข Neoplasms
Congenital

โ€ข Agenesis (very rare)
โ€ข Pancreas Divisum (failure of 2
ducts to fuse) (common)

โ€ข Annular Pancreas (pancreas
encircles duodenum) (rare)

โ€ข Ectopic Pancreas (very common)
PANCREATITIS
โ€ข ACUTE (VERY SERIOUS)
โ€ข CHRONIC (Calcifications,
Pseudocyst)
CONSEQUENCES of ACUTE and CHRONIC pancreatitis
ACUTE PANCREATITIS
โ€ข ALCOHOLISM
โ€ข Bile reflux
โ€ข
โ€ข
โ€ข
โ€ข
โ€ข
โ€ข

Medications (thiazides)
Hypertriglyceridemia, hypercalcemia
Acute ischemia
Trauma, blunt, iatrogenic
Genes: PRSS1, SPINK1
Idiopathic, 10-20%
CLINICAL FEATURES
โ€ข ABDOMINAL PAIN
โ€ข EXTREME emergency situation
โ€ข HIGH mortality
โ€ข โ€ฆbut MOST important lab test
isโ€ฆโ€ฆโ€ฆ.????? ๏ƒ 
AMYLASE
!!!!!!!
โ€ข
โ€ข
โ€ข
โ€ข
โ€ข
โ€ข

MORPHOLOGY

EDEMA
FAT NECROSIS
ACUTE INFLAMMATORY INFILTRATE
PANCREAS AUTODIGESTION
BLOOD VESSEL DESTRUCTION
โ€œSAPONIFICATIONโ€ (stearates, Na+,
Ca++)
CHRONIC PANCREATITIS
โ€ข Pancreatic duct obstruction,
LONGSTANDING
โ€ข Tropical
โ€ข Hereditary (PRSS1, SPINK1
mutations)
โ€ข IDIOPATHIC (40%)
CHRONIC PANCREATITIS
CLINICAL FEATURES
โ€ข Abdominal Pain
โ€ข Vague abdominal symptoms
โ€ข Nothing
โ€ข CT calcifications (why?), amylase
elevated, chronic diarrhea if chronic
pancreatic insuffiency develops, high
likelihood of pseudocysts
PDEUDOCYSTS
โ€ข Why โ€œpseudoโ€?
โ€ข STRONGLY linked with pancreatitis
โ€ข Can be as big as a football and often
are.
โ€ข Can cause obstruction
โ€ข Can get infected
โ€ข Do NOT become malignant
Pancreas Neoplasms
โ€ข
โ€ข
โ€ข
โ€ข
โ€ข
โ€ข
โ€ข

Serous
Mucinous
Cystic
Microcystic
Papillary
Benign
Malignant (dense sclerosis is the
rule)
SEROUS
CYSTADENOMA
MUCINOUS
CYSTADENOMA
INTRADUCTAL
PAPILLARY
MUCINOUS
โ€œNEOPLASMโ€
CARCINOGENESIS
of PANCREATIC
ADENOCARCINOMA
Pancreatic CA
Pancreatic
Adenocarcinoma
โ€ข
โ€ข
โ€ข
โ€ข

FATE:

Regional lymph nodes
Liver
Often L-2 spine
Lungs

Grading (WMP), Staging, TNM
Final TIP of the day
โ€ข Painless jaundice in an
elderly person is
CARCINOMA of the head
of the pancreas until
proven otherwise

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Minarcik robbins 2013_ch19-pancreas

Editor's Notes

  1. Perhaps the only thing thatโ€™s complicated about the pancreas, is its intimate relationship with the duodenum.
  2. The pancreas is the point in this course when I can start to see the light at the end of the tunnel!
  3. Know fates of dorsal and ventral buds.
  4. Know fates of dorsal and ventral buds.
  5. Know fates of dorsal and ventral buds.
  6. Know fates of dorsal and ventral buds. Now you know why the pancreas has TWO ducts!
  7. Know fates of dorsal and ventral buds.
  8. Know main anatomical landmarks and relationships to other organs
  9. Recall blood flow, arterial HEAD: Superior pancreatcoduodenal (A&P) arteries, from the gastroduodenal of the common hepatic of the CELIAC HEAD: Inferior pancreaticoduodenal (A&P) arteries from the SMA BODY and TAIL: SPLENIC
  10. โ€œPeri-โ€pancreatic lymph nodes, several groups.
  11. Pancreatic duct, the MAIN one from the VENTRAL bud, โ€œusuallyโ€ empties into the most distal portion of the CBD (Common Bile Duct)
  12. EGD (Esophago, Gastro, Duodenoscopy) This is where a GI doc might be able to remove a lodges stone, or biopsy an ampullary tumor.
  13. Axial diagram.
  14. Typical CT landmarks.
  15. Typical CT landmarks, with contrast.
  16. Histology concepts. Centroacinar๏ƒ intercalated๏ƒ intralobular๏ƒ interlobular
  17. H&E, e.m.
  18. Histology, H&E Find an intercalated duct.
  19. Classical classification again, our old friend.
  20. Pancreas Divisum is failure of fusion of dorsal and ventral buds.
  21. Why is the pancreas known as the most โ€œautolyticโ€ of all organs? What does autolytic mean? What happens if you wait a few days before doing an autopsy?
  22. Does this look like a partly digested piece of meat? It is.
  23. Why the blurr? Microscope out of focus. What is autolysis?
  24. Chronic pancreatitis goes hand in hand with chronic alcoholism.
  25. Find the โ€œsoapโ€, find the calcium.
  26. Unfortunately dense fibrosis is a feature BOTH of chronic pancreatitis as well as adenocarcinoma, but in pancreatitis, the fibrotic acini are usually still following a lobular pattern)
  27. What is every pathologistโ€™s nightmare? Ans: Getting a small needle biopsy of sclerosing pancreatitis and calling it it cancer on frozen section, getting the โ€œWhippleโ€ specimen the next day, and realizing you were WRONG! The patient has now undergone an operation which has a 10% mortality rate, for no reason, and the malpractice attorneys are at your door like jackals.
  28. Do you remember the anatomic area called the lesser sac?, also known as the omental bursa?
  29. Small pseudocyst, showing organizing inflamation on right
  30. Football sized pseudocyst, pretty much representing the entire lesser sac.
  31. These are also called โ€œmicroโ€-cystic, especially if the cysts are only easily recognized on microscopy.
  32. Various genetic alterations in the pathogenesis of pancreatic carcinoma. What to take home? Telomere shortening K-RAS mutations P16 inactivation Further inactivation of p53, SMAD4, BRCA2 More or less, in that order! This is a beautiful diagram because it correlates microscopic dysplastic changes with genetic alterations!
  33. Describe this in plain English.
  34. Gross fibrosis on left, microscopic on right.
  35. Perhaps โ€œbiologic behaviorโ€ is a better word than โ€œfateโ€?