Denning- Pancreas X 2- Leah Flashcards

1
Q

Where does the main pancreatic duct empty and what does it join?

Where does the accessory pancreatic duct drain?

A

Main: joins common bile duct; empties to duodenum at ampulla of vater
Accessory: small papillae slightly proximal to ampulla of vater

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2
Q

Common Requirement for activation for all pancreatic digestive enzymes? Inhibitory enzyme released with acinar and ductal secretion?

A
  • Duodenal enteropeptidase must cleave trypsinogen to trypsin
  • Inhibitory Eynzme: serine protease inhibitor Kalazal Type 1
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3
Q

Acinar epithelial cells:
Shape
Location
Function

A
  • Pyramidal shaped; radial orientation
  • outside of islets in ductal system
  • Secrete inert digestive enzymes; must be activated by proteases
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3
Q

How is the pancreas protected from enzymatic enzymes?

A

-enzymes inactive when released
AND
-acinar cells resistant to trypsin/chymotrypsin/PLase

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4
Q

Most severe congenital pancreatic condition?

Most common?

A

Agenesis- worst; incompatible with life

Pancreatic divisum- most common

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5
Q

Gene assc with pancreatic Agenesis?

A

PDX1; chromosome 13

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6
Q

What causes pancreatic divisum?
Where do pancreatic secretions drain?
Result?

A
  • Failure of dorsal and ventral buds to fuse
  • Secretions through small/ minor papillae
  • Small papillae overwhelmed –> stenosis –> chronic pancreatitis
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7
Q

Name for a pancreas encircling the duodenum?

How does it present?

A

Annular pancreas; duodenal obstruction

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8
Q

Ectopic pancreas:
Typical location?
Possible sequelae?

A

Stomach + duodenum

2% islet cell neoplasms are from ectopic tissue

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9
Q

Acute pancreatitis is a ________ process.

Chronic causes __________.

A

Acute: reversible
Chronic: irreversible loss exocrine + endocrine function

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10
Q

Top two causes of acute pancreatitis?
Which is seen mostly in males?
Mostly in females?

A

Alcoholism/ biliary tract disease (male) + gall stones (female)

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11
Q

GET SMASHED mnemonic for causes of acute pancreatitis?

A
  • Gall Stones
  • Ethanol
  • Trauma
  • Steroids
  • Mumps
  • AI disease
  • Scorpion Sting
  • Hyperlipidemia
  • Drugs
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12
Q

Pain described in acute pancreatitis?
What makes it worse or better?
Key lab findings? ***

A

Epigastric pain radiating to back
Relieve with doubling up
Worse with food

High amylase and lipase (not necessarily as pronounced in chronic)

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13
Q

Two genes assc with hereditary attacks of acute pancreatitis starting in childhood?

A

AD: cationic trypsinogen gene (PRSS1)
Trypsin resistant to cleavage

AR: serine protease inhibitor Kazal 1 (SPINK1)
Trypsin not inhibited

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14
Q

Appearance of a pancreas in acute pancreatitis?

5

A
  • Fat Necrosis
  • Calcium deposits
  • Hemorrhage (destroyed vasculature)
  • Edema
  • Proteolytic Parenchymal destruction
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15
Q

What is the final common cause of acute pancreatitis in all types?

A

Activation of pancreatic ENZYMES!

Can be induced by obstruction in stones/alcoholism, defective transport in alcoholism, or cell injury in all types

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16
Q

3 ways alcohol causes acute pancreatitis?

A
  • chronic ingestion = protein plugs –> obstruction
  • directly toxic
  • increased exocrine secretion
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17
Q

How is trypsin a bad actor in acute pancreatitis?

2 bad actions

A
  • Activates OTHER enzymes
  • -> fat and blood cells killed
  • Activates kinin system
  • -> clotting/complement
18
Q

How can fat necrosis effect lab values in acute pancreatitis?

A

Fatty acids combine with calcium –> LOW CALCIUM = BAD PROGNOSTIC SIGN *****

**Test Question ***

19
Q

How is disease severity predicted in acute pancreatitis?

A

Ransons criteria 48 HOURS AFTER ADMISSION

List that accounts for age/several labs etc

20
Q

Worst sequelae of acute pancreatitis?

A

ARDS –> vascular collapse –> shock and death

21
Q

4 other conditions to rule out when Dx’ing acute pancreatitis:

A
  • Ruptured appendix
  • perforated ulcer
  • ruptured gallbladder
  • bowel infarction
22
Q

Four poor prognostic factors in acute pancreatitis?

A
  • age
  • high white count
  • high glucose
  • low ca
23
Q

Class chronic pancreatitis patient?

A

Middle aged (AA?) alcoholic male

24
Q

Describe the gross and micro appearance of CHRONIC pancreatitis

A
  • Gross: hard glands with calcifications and pseudocysts

- Micro: fibrosis and destruction of ducts/acini

25
Q

Symptoms of chronic pancreatitis

A
  • repeated attacks of abdominal pain
  • jaundice
  • malabsorption/steatorrhea ***
26
Q

How does chronic pancreatitis develop?

A

Repeated Acute pancreatitis –> fibrosis, duct distortion, altered secretions

27
Q

Risk assc with chronic pancreatitis?

Treatment?

A

^^ risk pancreatitic cancer

Supportive exocrine enzymes, manage diabetes, steroid therapy

28
Q

Congenital cysts:
What do they look like?
What diseases are they assc with?

A

Unilocular, thin walled, serous filled
-VHL, ADPKD
(Can also be completely sporadic)

29
Q
Pseudocysts: 
How do they develop? 
How common? 
What, histologically, makes them "pseudo" cysts? 
Prognosis?
A

Inflammation of the pancreas –> collections of secretions
75% of pancreatic cysts
No epithelial lining
Great prognosis

30
Q

Serous cystadenoma:

  • benign or malignant
  • lining + filling
  • population
A

Benign
Cuboidal epi; straw fluid
Older females

31
Q

Mucinous cystic neoplasm of pancreas

  • population
  • important assc
  • location
  • lining/stroma/filling
A
  • 95% female
  • assc with invasive carcinoma
  • Body or tail
  • Columnar epi, ovarian stroma, filled with mucus

** dangerous and must be removed!**

32
Q

Intraductal Papillary Mucinous Neoplasm:

  • population
  • benign or malignant
  • gross appearance and location
  • key histo findings?
A
  • males
  • malignant
  • multilocular cyst in head
  • see papillae on histo; no ovarian stroma
33
Q
Solid pseudopapillary neoplasms: 
Male or female 
Prognosis 
Gross Appearance 
Histo
A
  • female
  • good prognosis
  • well circumscribed, large
  • filled with hemorrhagic debris
34
Q

Pancreatic carincoma

  • what type of carincoma?
  • common age and ethnicity?
  • deadly?
A
  • adenocarcinoma
  • blacks; older
  • 4th leading cause of cancer deaths
35
Q

Two modifiable risk factors for pancreatic cancer

Two assc genes

A

Smoking; high fat diet

KRAS; p53

36
Q

Hereditary diseases assc with pancreatic adenocarcinoma (4)

A

-BRCA2
-Peutz Jeghers
-Hereditary pancreatitis (PRSS1/ SPINK1)
- FAMILIAL ATYPICAL MULTIPE MOLE MELANOMA SYNDROME
(She had to have made this up)

37
Q

Precursor lesions of pancreas:

A

Pancreatic intraepi neoplasias

38
Q

MC location pancreatitic adenocarcinoma

Typical symptoms

A

Most in head

Usually asx until very late; then painless obstructive jaundice

39
Q

Pancreatic adenocarcinoma:

  • Gross appearance
  • Micro appearance
A
  • hard; grey white mass

- mitoses; necrosis; many cell types possible

40
Q

Describe trousseaus sign

A

Pancreatic carcinoma produces PAF –> migratory thrombophlebitis (only 10% cases)

41
Q

Pancreatic adenocarcinoma:
Treatment?
Prognosis?

A

Poor Prognosis!!!!!
20% can be resected by Whipple procedure
(Connect healthy pancreatic tissue to proximal duodenum + stomach to distal duodenum; take out tumor)

42
Q

Acinar cell carcinoma:

Appearance + secretions

A

-acinar cells. Secrete enzymes. = Metastatic fat necrosis (lipase)

43
Q

Pancreatoblastoma:

  • age group
  • benign v malignant?
  • appearance
A

Kids

Malignant squamous acinar cells (little blue cells)