Denning- Pancreas X 2- Leah Flashcards
Where does the main pancreatic duct empty and what does it join?
Where does the accessory pancreatic duct drain?
Main: joins common bile duct; empties to duodenum at ampulla of vater
Accessory: small papillae slightly proximal to ampulla of vater
Common Requirement for activation for all pancreatic digestive enzymes? Inhibitory enzyme released with acinar and ductal secretion?
- Duodenal enteropeptidase must cleave trypsinogen to trypsin
- Inhibitory Eynzme: serine protease inhibitor Kalazal Type 1
Acinar epithelial cells:
Shape
Location
Function
- Pyramidal shaped; radial orientation
- outside of islets in ductal system
- Secrete inert digestive enzymes; must be activated by proteases
How is the pancreas protected from enzymatic enzymes?
-enzymes inactive when released
AND
-acinar cells resistant to trypsin/chymotrypsin/PLase
Most severe congenital pancreatic condition?
Most common?
Agenesis- worst; incompatible with life
Pancreatic divisum- most common
Gene assc with pancreatic Agenesis?
PDX1; chromosome 13
What causes pancreatic divisum?
Where do pancreatic secretions drain?
Result?
- Failure of dorsal and ventral buds to fuse
- Secretions through small/ minor papillae
- Small papillae overwhelmed –> stenosis –> chronic pancreatitis
Name for a pancreas encircling the duodenum?
How does it present?
Annular pancreas; duodenal obstruction
Ectopic pancreas:
Typical location?
Possible sequelae?
Stomach + duodenum
2% islet cell neoplasms are from ectopic tissue
Acute pancreatitis is a ________ process.
Chronic causes __________.
Acute: reversible
Chronic: irreversible loss exocrine + endocrine function
Top two causes of acute pancreatitis?
Which is seen mostly in males?
Mostly in females?
Alcoholism/ biliary tract disease (male) + gall stones (female)
GET SMASHED mnemonic for causes of acute pancreatitis?
- Gall Stones
- Ethanol
- Trauma
- Steroids
- Mumps
- AI disease
- Scorpion Sting
- Hyperlipidemia
- Drugs
Pain described in acute pancreatitis?
What makes it worse or better?
Key lab findings? ***
Epigastric pain radiating to back
Relieve with doubling up
Worse with food
High amylase and lipase (not necessarily as pronounced in chronic)
Two genes assc with hereditary attacks of acute pancreatitis starting in childhood?
AD: cationic trypsinogen gene (PRSS1)
Trypsin resistant to cleavage
AR: serine protease inhibitor Kazal 1 (SPINK1)
Trypsin not inhibited
Appearance of a pancreas in acute pancreatitis?
5
- Fat Necrosis
- Calcium deposits
- Hemorrhage (destroyed vasculature)
- Edema
- Proteolytic Parenchymal destruction
What is the final common cause of acute pancreatitis in all types?
Activation of pancreatic ENZYMES!
Can be induced by obstruction in stones/alcoholism, defective transport in alcoholism, or cell injury in all types
3 ways alcohol causes acute pancreatitis?
- chronic ingestion = protein plugs –> obstruction
- directly toxic
- increased exocrine secretion
How is trypsin a bad actor in acute pancreatitis?
2 bad actions
- Activates OTHER enzymes
- -> fat and blood cells killed
- Activates kinin system
- -> clotting/complement
How can fat necrosis effect lab values in acute pancreatitis?
Fatty acids combine with calcium –> LOW CALCIUM = BAD PROGNOSTIC SIGN *****
**Test Question ***
How is disease severity predicted in acute pancreatitis?
Ransons criteria 48 HOURS AFTER ADMISSION
List that accounts for age/several labs etc
Worst sequelae of acute pancreatitis?
ARDS –> vascular collapse –> shock and death
4 other conditions to rule out when Dx’ing acute pancreatitis:
- Ruptured appendix
- perforated ulcer
- ruptured gallbladder
- bowel infarction
Four poor prognostic factors in acute pancreatitis?
- age
- high white count
- high glucose
- low ca
Class chronic pancreatitis patient?
Middle aged (AA?) alcoholic male
Describe the gross and micro appearance of CHRONIC pancreatitis
- Gross: hard glands with calcifications and pseudocysts
- Micro: fibrosis and destruction of ducts/acini
Symptoms of chronic pancreatitis
- repeated attacks of abdominal pain
- jaundice
- malabsorption/steatorrhea ***
How does chronic pancreatitis develop?
Repeated Acute pancreatitis –> fibrosis, duct distortion, altered secretions
Risk assc with chronic pancreatitis?
Treatment?
^^ risk pancreatitic cancer
Supportive exocrine enzymes, manage diabetes, steroid therapy
Congenital cysts:
What do they look like?
What diseases are they assc with?
Unilocular, thin walled, serous filled
-VHL, ADPKD
(Can also be completely sporadic)
Pseudocysts: How do they develop? How common? What, histologically, makes them "pseudo" cysts? Prognosis?
Inflammation of the pancreas –> collections of secretions
75% of pancreatic cysts
No epithelial lining
Great prognosis
Serous cystadenoma:
- benign or malignant
- lining + filling
- population
Benign
Cuboidal epi; straw fluid
Older females
Mucinous cystic neoplasm of pancreas
- population
- important assc
- location
- lining/stroma/filling
- 95% female
- assc with invasive carcinoma
- Body or tail
- Columnar epi, ovarian stroma, filled with mucus
** dangerous and must be removed!**
Intraductal Papillary Mucinous Neoplasm:
- population
- benign or malignant
- gross appearance and location
- key histo findings?
- males
- malignant
- multilocular cyst in head
- see papillae on histo; no ovarian stroma
Solid pseudopapillary neoplasms: Male or female Prognosis Gross Appearance Histo
- female
- good prognosis
- well circumscribed, large
- filled with hemorrhagic debris
Pancreatic carincoma
- what type of carincoma?
- common age and ethnicity?
- deadly?
- adenocarcinoma
- blacks; older
- 4th leading cause of cancer deaths
Two modifiable risk factors for pancreatic cancer
Two assc genes
Smoking; high fat diet
KRAS; p53
Hereditary diseases assc with pancreatic adenocarcinoma (4)
-BRCA2
-Peutz Jeghers
-Hereditary pancreatitis (PRSS1/ SPINK1)
- FAMILIAL ATYPICAL MULTIPE MOLE MELANOMA SYNDROME
(She had to have made this up)
Precursor lesions of pancreas:
Pancreatic intraepi neoplasias
MC location pancreatitic adenocarcinoma
Typical symptoms
Most in head
Usually asx until very late; then painless obstructive jaundice
Pancreatic adenocarcinoma:
- Gross appearance
- Micro appearance
- hard; grey white mass
- mitoses; necrosis; many cell types possible
Describe trousseaus sign
Pancreatic carcinoma produces PAF –> migratory thrombophlebitis (only 10% cases)
Pancreatic adenocarcinoma:
Treatment?
Prognosis?
Poor Prognosis!!!!!
20% can be resected by Whipple procedure
(Connect healthy pancreatic tissue to proximal duodenum + stomach to distal duodenum; take out tumor)
Acinar cell carcinoma:
Appearance + secretions
-acinar cells. Secrete enzymes. = Metastatic fat necrosis (lipase)
Pancreatoblastoma:
- age group
- benign v malignant?
- appearance
Kids
Malignant squamous acinar cells (little blue cells)
