1. PANCREAS

4. OBJECTIVES
Understand the etiology/risk factors, pathogenesis, morphology, clinical features and outcome of pancreatic inflammations and neoplasms

5. Know fates of dorsal and ventral buds.

6. Know fates of dorsal and ventral buds.

7. Know fates of dorsal and ventral buds.

8. Know fates of dorsal and ventral buds.

9. Know fates of dorsal and ventral buds.

10. Chapter 19

11. Posterior view of duodenum/pancreas
Know main anatomical landmarks and relationships to other organs

12. Arterial supply and venous drainage of the pancreas and spleen
Recall blood flow, arterial, venous.

13. Lymphatic drainage of the distal pancreas and spleen
“Peri-”pancreatic lymph nodes, several groups.

14. Pancreatic duct, the MAIN one from the VENTRAL bud, “usually” empties into the most dstal portion of the CBD (Common Bile Duct)

15. Hepaticopancreatic ampulla (Ampulla of Vater)
EGD (Esophago, Gastro, Duodenoscopy)

16. Axial diagram.

17. Typical CT landmarks.

18. Typical CT landmarks, with contrast.

19. Histology concepts.

20. H&E, e.m.

21. Histology, H&E

22. Pancreatic Enzymes Amylase Lipase DNA-ase RNA-ase
Zymogens: Trypsinogen Chymotrypsinogen, Procarboxypeptidase A, B

23. Inflammatory Neoplasms PANCREAS DISEASES Congenital Cysts Acute
Chronic
Cysts
Neoplasms
Classical classification again, our old friend.

24. Congenital Agenesis (very rare)
Pancreas Divisum (failure of 2 ducts to fuse) (common)
Annular Pancreas (pancreas encircles duodenum) (rare)
Ectopic Pancreas (very common)

27. PANCREATITIS
ACUTE (VERY SERIOUS)
CHRONIC (Calcifications, Pseudocyst)

28. CONSEQUENCES of ACUTE and CHRONIC pancreatitis

29. ACUTE PANCREATITIS ALCOHOLISM Bile reflux Medications (thiazides)
Hypertriglyceridemia, hypercalcemia
Acute ischemia
Trauma, blunt, iatrogenic
Genes: PRSS1, SPINK1
Idiopathic, 10-20%

30. CLINICAL FEATURES ABDOMINAL PAIN EXTREME emergency situation
HIGH mortality
…but MOST important lab test is……….????? 

31. AMYLASE
!!!!!!!

32. MORPHOLOGY EDEMA FAT NECROSIS ACUTE INFLAMMATORY INFILTRATE
PANCREAS AUTODIGESTION
BLOOD VESSEL DESTRUCTION
“SAPONIFICATION”

33. Does this look like a partly digested piece of meat? It is.

34. Why the blurr? Microscope out of focus. What is autolysis?

35. CHRONIC PANCREATITIS Pancreatic duct obstruction, LONGSTANDING
Tropical
Hereditary (PRSS1, SPINK1 mutations)
IDIOPATHIC (40%)
Chronic pancreatitis goes hand in hand with chronic alcoholism.

36. Find the “soap”, find the calcium.

37. Unfortunately dense fibrosis is a feature BOTH of chronic pancreatitis as well as adenocarcinoma.

38. What is every pathologist’s nightmare
What is every pathologist’s nightmare? Ans: Getting a small needle biopsy of sclerosing pancreatitis and calling it it cancer, getting the “Whipple” 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 at at your door like jackals.
CHRONIC PANCREATITIS

39. CLINICAL FEATURES Abdominal Pain Vague abdominal symptoms Nothing
CT calcifications (why?), amylase elevated, chronic diarrhea if chronic pancreatic insuffiency develops, high likelihood of pseudocysts

40. PDEUDOCYSTS Why “pseudo”? STRONGLY linked with pancreatitis
Can be as big as a football and often are.
Can cause obstruction
Can get infected
Do NOT become malignant

41. Small pseudocyst, showing organizing inflamation on right

42. Football sized pseudocyst, pretty much representing the entire lesser sac.

43. Pancreas Neoplasms Serous Mucinous Cystic Microcystic Papillary Benign
Malignant (dense sclerosis is the rule)

44. SEROUS
CYSTADENOMA
These are also called “micro”-cystic, especially if the cysts are only easily recognized on microscopy.

45. MUCINOUS
CYSTADENOMA

46. INTRADUCTAL
PAPILLARY
MUCINOUS
“NEOPLASM”

47. CARCINOGENESIS of PANCREATIC ADENOCARCINOMA
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!

48. Pancreatic CA
Describe this in plain English.

49. Pancreatic Adenocarcinoma
Gross fibrosis on left, microscopic on right.

50. FATE: Regional lymph nodes Liver Often L-2 spine Lungs
Grading (WMP), Staging, TNM
Perhaps “biologic behavior” is a better word than “fate”?

51. Final TIP of the day
Painless jaundice in an elderly person is CARCINOMA of the head of the pancreas until proven otherwise