Pancreas Flashcards

1
Q

What is the most common congenital anomaly of pancreas

A

Pancreas divisum.
Failure of fusion of dorsal and ventral pancreatic buds

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2
Q

Which structures Opens at ampulla of vater.

A

Main pancreatic duct (Wirsung duct) + CBD opening

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3
Q

Distal part of accessory duct of Santorini

A

Opens at minor papilla.

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4
Q

What is Annular pancreas :

A

• malrotation of the ventral bud of pancreas -> Encircles 2ndpart of duodenum -> Annular pancreas.

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5
Q

C/f of annular pancreas

A

Non bilious vomiting

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6
Q

Which sign is seen on X-Ray of annular pancreas

A

Double bubble sign (also seen in duodenal atresia)

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7
Q

IOC and Management of duodenal atresia

A

IOC : CECT abdomen
Management: Duodenoduodenostomy (DD)

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8
Q

Sphincter of oddi made of how many sphincter

A

4 Sphincter

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9
Q

Which classification is used for sphincter of oddi dysfunction

A

Milwaukke classification

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10
Q

MCC of acute pancreatitis

A

Gall stone induced
(2nd most is alcohol)

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11
Q

MCC of acute pancreatitis in children

A

Blunt trauma to abdomen

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12
Q

Pathophysiology of pancreatitis

A

Any stimulus -> Increased calcium -> co-localization of zymogen and lysosome -> Fuse -> Trypsinogen releases cathepsin B -> Activate trypsin -> Acinar death :
Inflammatory cascade.

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13
Q

Inflammatory mediators of pancreatitis are

A

IL I, IL 6, TNF alpha, IL 10.

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14
Q

CF of acute pancreatitis

A
  1. Pain epigastrium radiating to back, relieved on bending forward.
  2. out of proportion symptoms.
  3. Features of peritonitis: Guarding, rigidity, rebound tenderness (severe pancreatitis)
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15
Q

Sings in acute hemorrhagic pancreatitis

A

Cullen’s sign ;
Grey turner sign ;
Fox sign :

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16
Q

Describe Cullen’s sign

A

Discoloration around umbilicus.

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17
Q

Grey Turner’s sign

A

Discoloration in flanks.

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18
Q

• Fox sign:

A

Discoloration in inguinal region.

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19
Q

Discoloration is due to

A

Retroperitoneal bleeding

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20
Q

Diagnosis of pancreatitis is made by

A

I. Abdominal pain consistent with pancreatitis.
2. >/= 3 fold high elevated serum amylase/lipase above upper laboratory levels.
3. Characteristic findings of pancreatitis by imaging.
If any 2 of the above positive -> Pancreatitis.

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21
Q

Serum amylase in acute pancreatitis is

A

Rises quickly, shorter half life, sensitive.

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22
Q

Serum lipase in acute pancreatitis is

A

Rises gradually, longer half life, more specific. Amylase and lipase not predictive of severity of attack.

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23
Q

IOC For Acute Pancreatitis

A

CECT abdomen.
• Done after 72 hours after onset of symptoms.
• If within 72 hours, it can underestimate the severity.
• Portal venous phase in CECT
(65-70 seconds after contrast): most sensitive for pancreatitic necrosis.

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24
Q

Radiological signs in acute pancreatitis

A

Colon cut off sign (ileus) on X-ray.
Sentinel loop sign (focal dilated jejunal loop).
Gasless abdomen (also seen in acute gastroenteritis, diarrhea).

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25
Q

Glasgow criteria is valid for

A

Both gallstone and alcohol induced pancreatitis.
>/= 3 severe pancreatitis

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26
Q

Ranson score is valid for

A

Alcohol induced pancreatitis.

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27
Q

Glasgow criteria includes

A

PANCREAS

It is scored through the mnemonic, pancreas:
• P: PaO2 < 8 KPa.
• A: Age > 55 years old
• N: Neutrophilia: WCC >15 x 10^9/L.
• C : Calcium < 2 mmol/L.
• R: Renal function, urea > 16 mmol/L.
• E: Enzymes : LDH > 6OOiu/L ;
AST > 200iu/L.
• A : Albumin < 3.2g/L (serum).
• S: Sugar: Blood glucose >10 mmol/L.

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28
Q

BISAP Score includes

A

BUN > 25 mg / dl
Impaired mental status
SIRS
Age >60
Pleural effusions

> /=3 indicates severe pancreatitis

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29
Q

Other markers for pancreatitis

A
  1. C-reactive protein > 150 IU/L : Severe pancreatitis.
  2. APACHE system: Acute physiology and chronic health evaluation score (>/= 8 : Severe pancreatitis).
  3. APACHE O score: (0-obesity).
  4. HAPS score harmless acute pancreatitis score).
  5. modified marshall’s score:
    • Tells about organ dysfunction.
    • >/= 2: Organ dysfunction.
  6. Balthazar grading : Best scoring system for acute pancreatitis (CT severity index).
    • >/= 6: severe pancreatitis.
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30
Q

What is pancreatic ascetics

A

Disruption of pancreatic duct

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31
Q

What is the most common vessel involved in vascular complication of pancreatic necrosis

A

Splenic artery

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32
Q

What is chronic pancreatitis?

A

Repeated attacks of pancreatitis -> Fibrosis + chronic inflammation -> irreversible damage to pancreatic parenchyma (single/multiple episodes).

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33
Q

What is the MCC of Chronic pancreatitis (tigaro classification)

A

Alcohol

34
Q

Genes associated with chronic pancreatitis

A
  1. PRSS I (Chromosome 7) : Protease serine I gene - hereditary chronic pancreatitis.
    • Increases risk of cancer.
  2. SPINKI: Peptide secreted by acinar cells that regulates premature activation of trypsinogen.
    • Associated with tropical calcific pancreatitis : Cassava ingestion.
  3. CFTR gene : Heterozygous
    - mutation predisposes to chronic pancreatitis.
    • CFTR gene: Homogeneous mutation -> Cystic fibrosis.
35
Q

What is burnt out pancreas

A

Pain subsides as destruction increases (acini die off)

36
Q

IOC for chronic pancreatitis

A

MRCP with secretin simulation (chain of lakes appearance, if there are multiple stones in pancreatic duct)

37
Q

Gold standard investigation in chronic pancreatitis

A

ERCP

38
Q

What to do with the size of Maine pancreatic duct is >5 MM

A

Anastomose ;
1) duval method
2) puestow procedure

39
Q

What is duval method

A

End to end pancreatico - jejunal anastomosis

40
Q

What is puestow procedure

A

AKA longitudinal pancreatico jejunostomy. Entire length of pancreatic duct is anastomose with jejunum side to side.

41
Q

What is Bergers procedure ?

A

Duodenal preserving pancreatic head resection

42
Q

What is frey method

A

Puestow’s + Berger’smethod:

Done when pancreatitis is restricted to head and stones all along the duct.

43
Q

Explain Serous cystic neoplasm

A

• More common in head.
• Older patients.
• Glycogen rich cells are seen.
• CEA are not raised.
• Large; multiloculated masses
• usually benign.

44
Q

In CT of serous cystic neoplasm what can be seen

A

Sunburst appearance on CT due to central calcification and septae being given off

45
Q

what is Ohashi Triad

A

• Dilated Hepatopancreatic duct.
• mucin coming out from the ampullary opening.
• Fish mouth appearance.

46
Q

Solid pseudopapillary tumour/ Gruber Frantz tumour is known as

A

Hamoudi Tumour.
Commonly seen in the tail of the pancreas. Malignant lesion but slowly progressing

47
Q

Which syndrome is associated with PRSS1 gene

A

Familial pancreatitis

48
Q

Which syndrome is associated with STK11 gene

A

Peutz Jeghers syndrome

49
Q

Which syndrome is associated with CDKN2A gene

A

Familial atypical mole and multiple melanoma syndrome.

50
Q

Which syndrome is associated with CFTR gene

A

Cystic fibrosis

51
Q

Which syndrome is associated with BRAC2 gene

A

Hereditary breast and ovarian

52
Q

Most common gene mutated in pancreatic cancer

A

K-RAS

53
Q

What is Periampullary carcinoma

A

Are a group of 4 cancers within 2 cm of ampullary opening.
All of these have similar features and presentation.

54
Q

What is the mc presentation of pancreatic carcinoma

A

Progressive Obstructive jaundice

55
Q

What is Courvoisier’s law

A

Obstructive jaundice with palpable gallbladder is seldom due to stone disease. It is mostly due to cancer.
In cancer when there is blockage distally in the CBD, the CBD will dialate.
As a result of which there is gallbladder distention. when a stone blocks the CBD distally, the gallbladder will not be palpable instead it will be shrivelled due to inflammatory fibrosis.

56
Q

Which sign is seen on duodenography in pancreatic ductal carcinoma

A

Frosberg Reverse 3 Sign

57
Q

Which sign is seen on MRCP/ERCP in pancreatic ductal carcinoma

A

Double duct sign this occurs because of the obstruction at the ampullary opening, the CBD is compressed and the ampullary opening is also compressed as a result of which both the structures get dilated

58
Q

What is the predictive and prognostic marker of pancreatic carcinoma

A

CA-19-9

59
Q

Modified Whipple’s / Longmire and Traverso procedure is done in all cases except

A
  1. If duodenum is involved.
  2. If negative margins cannot be attained.
60
Q

Which incision is made if the tumor is located in the head of pancreas

A

Chevron or Rooftop incision

61
Q

Which structures are cut in the Modified Whipple’s /Longmire and Traverso procedure

A
  1. Transected the pylorus.
  2. CBD is resected and a cholecystectomy is done.
  3. Head and neck with part of Body of the pancreas.
  4. Duodenum.
62
Q

Which parts are left after the resection

A

After resection the parts left are :
I. Cut end of CBD.
a. Cut end of gallbladder.
3. Cut end of pancreas.
4. Jejuneum.

63
Q

What is the tunnel of love

A

Plane which is present between the vessel and the pancreas

64
Q

Steps of whipple’s surgery

A
  1. The plane “tunnel of love” is formed.
  2. Body is resected.
  3. Retroperitoneal mobilization of the pancreas
  4. Cupping of pancreatic head , proximal jejunum and duodenum.
  5. Ligation of inferior pancreaticoduodeenal vessels
  6. The ligament of Trierz is cut
  7. Mobilization of the jejunum through the transverse mesocolon window
  8. Uncinate is dissected under the confluence of the superior mesenteric vein and portal vein lateral to SMA.
    9.Stomach is dissected and stapled.
  9. Cholecystectomy is done(fundus first method)
  10. CBD is clamped (with the help of a bulldog clamp) and resected.
  11. Head of pancreas tumor specimen is sent to the pathologist .
  12. The 3 anastomosis is done.
65
Q

MC complication following whipples procedure is

A

Impaired gastric emptying due to loss of receptive relation of the stomach following vagotomies and Whipple’s surgery.

66
Q

MC cause of death in patient following whipple’s is

A

Anastomosis leak

67
Q

Which chemotherapy regime has better survival than only gemcitabine

A

mFOLFIRINOX

68
Q

What is the most common pancreatic endocrine neoplasm

A

Insulinoma (but the incidence of insulinoma is much less than ductal adenocarcinoma)

69
Q

Whipple’s triad includes

A

Fasting hypoglycaemia.
Low blood glucose value (<50mg/dL).
Rapid resolution on giving glucose.
Weight gain.

70
Q

How to differentiate patients who have insulinoma from those who has excess exogenous insulin?

A

In insulinoma, the C-peptide values will be raised : > 1.2 micrograms/ml.
Whereas in case of excess insulin administration of C-peptid values will not be raised.

71
Q

How does Diazoxide helps in management of insulinoma

A

Inhibits the release of insulin from β cells. Can be used to manage a person before surgery to prevent hypoglycemia.

72
Q

What is the most common site of Metastasis in case of malignant insulinoma

A

Liver

73
Q

What is the Most common pancreatic endocrine tumor in MEN1 syndrome

A

Gastrinoma/ Zollinger Ellison syndrome

74
Q

Gastrinoma (gastric sec tumor) arising from

A

Passaro’s triangle

75
Q

Boundaries of Passaro’s triangle

A
  1. Junction of cystic duct with common hepatic duct.
  2. Head and neck with body of pancreas.
  3. Junction of second part of duodenum with 3rd part of duodenum.
76
Q

Contents of Passaro’s triangle

A

• Superior and descending duodenum.
(DI, part of Da).
• Head of pancreas.
• Lymph nodes.

77
Q

What is the most common site of Gastrinoma

A

Wall of D1

78
Q

Zoolinger Ellison Triad includes

A

I. Increased gastrin.
2. Increased acid output.
3. Non beta cell tumour.

79
Q

Glucagonoma arises from

A

α cell of the islet of langerhans

80
Q

What are the 4D’s in glucagonoma

A

• Diabetes mellites.
• Dermatitis: Necrolytic migratory rash.
This rash occurs due to ammino acid deficiency. infusion of amino acids is administered the rash sub-sides.
• DVT.
• Depression.

81
Q

What is WDHA syndrome / verner morrison syndrome.

A

seen in a VIPoma (vasoactive intestinal peptide)
WD: Watery diarrhoea
H : Hypokalaemia
A : Achlorhydria, acidosis.

82
Q

The features non - functional tumour can be differentiated from a functional tumour are :

A

Increase chromogranin and synaptophysin.
Presents with abdominal pain, jaundice and mass abdomen.