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MedEd + PathSoc + Laz's Qs + Romesh Path > Histopathology 9: Pancreas & Gall Bladder > Flashcards

Histopathology 9: Pancreas & Gall Bladder Flashcards

1
Q

Which 2 mediators control enzyme and alkali release from the pancreas ?

A

Secretin - released by S cells in the duodenum causes pancreatic HCO3- secretion

Cholecystokinin (CCK) - released by I cells in the duodenum causes pancreatic release of digestive enzymes

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2
Q

Which cells release glucagon ?

A

Alpha cells

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3
Q

Which cells release somatostatin ?

A

Delta cells

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4
Q

What type of hypersensitivity reaction is T1DM ?

A

Type 4 delayed T cell mediated

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5
Q

List the causes of Acute pancreatitis ?

A

I GET SMASHED

Duct obstruction -> gallstones, trauma, tumours (MAIN SO REMEMBER)

Metabolic -> alcohol, drugs (thiazides), hypercalcaemia (COMES UP IN EXAMS), hyperlipidaemia

Poor blood supply -> Shock and hypothermia

Infection -> Mumps

AI

Idiopathic

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6
Q

Which blood test is most sensitive for Acute pancreatitis ?

A

Serum Lipase

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7
Q

List 4 causes of chronic pancreatitis ?

A

Cystic fibrosis
Alcoholism
Pancreatic duct obstruction - stones /cancer
Auto-immune

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8
Q

Describe the histology of chronic pancreatitis ?

A
  • Dilated ducts
  • Fibrosis
  • calcification
  • loss of exocrine tissue
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9
Q

A patient presents with significant weight loss, abdominal pain, multifocal fat necrosis and polyarthralgia. Histopathology: Eosinophilic granular cytoplasm, immune reactivity for lipase

Most likely diagnosis ?

A

Acinar cell carcinoma

neoplasm that releases lots of lipase

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10
Q

A patient presents with epigastric pain that radiates to the back, he’s jaundiced and appears cachectic. An abdominal mass is felt on examination.

Most likely diagnosis ?

A

Ductal adenocarcinoma of the pancreas

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11
Q

Where in the pancreas do Ductal adenocarcinomas tend to occur ?

A

Head of the pancreas

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12
Q

What is covosiers law ?

A

Presence of a palpable enlarged gallbladder, with painless jaundice means gallstones are unlikely.

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13
Q

What is the tumour marker for pancreatic cancer ?

A

CA19-9

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14
Q

Histopathology: Cells arranged in nests or trabecular with granular cytoplasm.

Most likely diagnosis ?

Characteristic feature?

A

Islet cell tumour- Insulinoma

Hypoglycaemic attacks.

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15
Q

Which syndrome is associated with gastrinomas

A

Zollinger ellison syndrome

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16
Q

What are Rokitansky-Aschoff sinuses ?

A

Cholecystitis causes fibrosis which means the gallbladder is contracting against an obstruction.

This pressure causes diverticula of the gallbladder to form which are known as Rokitansky-Aschoff sinuses.

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17
Q

What is the endocrine /exocrine aspect of the pancreas?

What do they produce?

A

Endocrine - Islet of Langerhands:
Insulin
Glucagon
Somatostatin

Exocrine - Acini + ducts:
Protease
Lipase
Amylase

18
Q

Define acute pancreatitis

A

Acute inflammation of the pancreas caused by aberrant release of pancreatic enzymes

19
Q

How do alcohol, gallstones and other causes of acute pancreatitis cause it?

Note this is also how chronic pancreatitis works

A

Alcohol: (Duct obstruction)
Spasm/oedema of the sphincter of Oddi + formation of protein-rich pancreatic fluid which is thick and causes an obstruction

Gallstones: (Duct obstruction)
Get stuck distal to where CBD and pancreatic duct join
→ bile reflux up pancreatic duct → damage to acini → release of proenzymes which then become activated

All other causes:
Via direct acinar injury

20
Q

Describe the three main patterns of injury in acute pancreatitis and describe what they result from.

A

Periductal – necrosis of acinar cells near ducts (usually secondary to obstruction)

Perilobular – necrosis at the edges of the lobules (usually due to poor blood supply)

Panlobular – results from worsening periductal or perilobular inflammation

21
Q

Outline the pathway of inflammation in acute pancreatitis

A

Activated enzyme reflux 🡪 acinar necrosis 🡪 release of more enzymes

Release of lipases 🡪 fat necrosis 🡪 saponification w/ calcium (soaps formed when ca binds w/ free fatty acids)

22
Q

Complications of acute pancreatitis v chronic pancreatitis? (4)

A

Acute:

  • Pseudocyst formation, abscesses
  • Shock
  • Hypoglycaemia
  • Hypocalcaemia (due to saponification)

Chronic:

  • Malabsorption
  • Diabetes mellitus
  • Pseudocysts
  • Pancreatic carcinoma
23
Q

What are pseudocysts?

What happens to pseudocysts?

A

A collection of fluid in a dilated space without an epithelial lining (has fibrous lining)

They are rich in pancreatic enzymes and necrotic material

They are lined by fibrous tissue

NOTE: they may resolve, compress adjacent structures, become infected or perforate (if they perforate → necrotic material rich in activated enzymes leaks into peritoneal cavity = acute peritonitis)

24
Q

What is the characteristic feature of autoimmune pancreatitis?

How is this treated?

A

Large numbers of IgG4 positive plasma cells typically found around the ducts

Steroids - usually responds well

25
Q

Different types of pancreatic tumours?

A

Carcinomas:
Ductal (85%)
Acinar (15%)

Note: acinar-ductal metaplasia (most originate from acinar-> ductal carcinoma - true ductal looks different)

Cystic neoplasms:
Serous cystadenoma (assc w von-hipel-lindau)
Mucinous cystic neoplasm

Neuroendocrine islet cell tumours:
Insulinoma (MOST COMMON)
Gastrinoma
VIPoma

26
Q

DIfferent types of MEN?

A

Multiple Endocrine Neoplasia (MEN)

A group of genetic syndromes where there are functioning hormone-producing tumours in multiple
organs e.g;
• MEN 1= ‘PPP’ - Parathyroid hyperplasia/adenoma, Pancreatic endocrine tumour (often phaeochromacytoma -adrenal), Pituitary adenoma.
• MEN 2A- Parathyroid, Thyroid, phaeochromacytoma
• MEN 2B- Meduallary Thyroid, Phaeo, Neuroma. Marfanoid phenotype

27
Q

What are the two types of gallstone and what are their distinguishing features? how many? radiolucency?

A

Cholesterol

  • May be single
  • Mostly radiolucent (NOT seen on AXR)

Pigment

  • Often multiple
  • Contain calcium salts of unconjugated bilirubin
  • Mostly radio-opaque
28
Q

Most common site of duct carcinoma?

What happens in the other place?

A

Head (60%)

NOTE: neuroendocrine tumours are more common in the tail

29
Q

Which mutation is very common in pancreatic cancer?

A

K-ras (95%)

30
Q

Name two types of dysplastic precursor lesion that ductal carcinoma can arise from.

A

Pancreatic intraductal neoplasia (PanIN)

Intraductal mucinous papillary neoplasm (IMPN)

31
Q

Microscopic and macroscopic appearances of ductal carcinoma?

Which cancers present earlier?

A

Microscopic:

  • Adenocarcinomas (secrete mucin and form glands)
  • Mucin-secreting glands are set in desmoplastic stroma

Macroscopic:

  • Gritty and grey
  • Invades adjacent structures

NOTE: tumours in the head of the pancreas present earlier

32
Q

where are mucin-secreting glands in adenocarcinomas?

A

Mucin-secreting glands set in desmoplastic stroma (means: strong stromal reaction)

33
Q

Recall a neuroendocrine marker in pancreatic endocrine neoplasms

A

Chromogranin

34
Q

In which portion of the pancreas are neuroendocrine tumours most common?

A

Tail

35
Q

Cholecystitis causes?

A

Acute (MAIN ONE IN Qs)

  • Acute inflammation
  • Associated w/ gallstones

Chronic:

  • Chronic inflammation
  • Fibrosis
  • Associated w/ gallstones
36
Q

What are the two most common causes of acute pancreatitis? Complications?​

A

Gallstones, alcohol -> pseudocyst, abscess, chronic pancreatitis​

37
Q

Which cells are involved in autoimmune pancreatitis?​

A

IgG4 plasma cells​

38
Q

What is the precursor lesion for a pancreatic ductal carcinoma?​

A

PANin (pancreatic intraductal neoplasms)​

39
Q

Which genetic syndrome is most commonly associated with pancreatic endocrine neoplasms?​

A

MEN1​

40
Q

What are gallstones most commonly composed of?​

A

Cholesterol

MedEd + PathSoc + Laz's Qs + Romesh Path (99 decks)

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