Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Year 5 Path Histopathology > Pancreas and Gall Bladder > Flashcards

Pancreas and Gall Bladder Flashcards

1
Q

Recall the normal anatomy of the pancreas

A
  1. Endocrine (Islet of Langerhans) and exocrine (acini) sections.
  2. Exocrine secretions go via different ducts (intercalated, interlobular, main pancreatic, common bile) to enter duodenum
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are the main causes of acute pancreatitis?

A
  1. Duct blockage –> 50% caused by Gallstotnes (+trama and tumours)
  2. Metabolic/toxic –> alcohol (2nd most common cause, 1/3) 5% of alcoholics will get acute pancreatiti, + drugs, hypercalcaemia and hyperlipidaemia
  3. ischaemic
  4. Infection/inflammation viruses (mumps)
  5. autoimmune - IgG4
  6. Idiopathic 15%
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

How does duct obstruction cause acute pancreatitis?

A

Reflux of bile followed by damage to acini activates pancreatic pro-enzymes –> damage to acini –> more release of pancreatic pro-enzymes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

How doe alcohol cause acute pancreatitis?

A

Alcohol leads to spasm/oedema of Sphincter of Oddi and the formation of a protein rich pancreatic fluid which obstructs the pancreatic ducts

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is the pattern of inflammation in acute pancreatitis with alcohol or gall-stones?

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 – develops from 1. and 2

  1. Release of enyzmes cause acinar necrosis –> oedema / haemorrhagig necrosis
  2. FAT NECROSIS (due to release of lipase binding to calcium)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What histological features indicate acute pancreatitis?

A
  1. stromal oedema - haemorrhagic necroris
    2.Fat necrosis (lipases bind go calcium) (blue areas)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What are the local and systemic complication sof acute pancreatitis?

A

Local complications:

  • pseudocyst, abscess

Systemic

  • shock
  • hypoglycaemia
  • hypocalcaemia (due to fat necrosis formation but can appear normocalcaemia if hypercalaemia was cause of pancreatitis in the first place)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is the prognosis of an episode of acute pancreatitis?

A

Up to 50% mortalitiy in haemorrhagic pancreatitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are the main causes of chornic pancreatitis?

A

Alcohol 80%
Haemochromatosis

+ Duct obstructions (potentially gallstones, abnormal pancreatic duct anatomy
+ or cystic fibrosis

Idiobpathic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are the histological changes seen in chronic pancreatitis?

A
  1. chornic inflammation –> lymphocytes with parenchymal fibrosis (hallmark) and loss of parenchyma (usually of acini, less of ilslands) , might be calcified (vs acute fat necrosis)
  2. Duct structures with calcified stones with secondary dilatations

Picture–> show fibrosis and islands of langerhans (might look like neuro-endocrine tumour)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is a pancreatic pseudo cyst?

What is their aetiology, definition, and complications?

A

Can be formed b y acute or chronic pancreatitis

Lined by fibrous tissue (no epithelial lining), contain fluid rich in pancreatic enzymes or necrotic material

Connect with pancreatic ducts

May resolve, compress adjacent structures, become infected or perforate (if perforation –> rlease of pancreatic enzymes, dangerous)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is IgG4 related pancreatitis?

A

Autoimmune pancreatitis
IgG4 related diseas is a disease in of itself causing inflammation pretty much anywhere in the body

Characterised by large numbers of IgG4 positive plasma cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is the most common pancreatic cancer?

What other malginancies can arise=?

A

Most: ductal caricinoma (small % acini carcinom)

Other possible, more rare:

  • Cystic neoplasm (serous + mucinous)
  • Pancreatic neuroendocrine tumours (islet cell)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is the pre-malignant stage of ductal carinomas of the pancrease?

What is the main genetic mutation driving it?

A

Usually 2
1. PanIN (pancreatic intraductal neoplasia)
2. Intrductal Mucinous Papillary Neoplasm

95% have K-ras mutation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is the main macroscopic and microscopic appearance of ductal carcinomas in the pancreas?

A
  1. Macroscopic: Gritty and grey
    Invades adjacent structures
    Tumours in the head present earlier

Microscopic
Adenocarcinomas:
mucin secreting glands set in desmoplastic stroma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are the main sites of pancreatic carcinomas?

A

60% are in the head
Body
Tail
Diffuse

17
Q

What are the main causes of ductal carcinomas of the pancreas?

A
  • Due to spread
  • Chronic pancreatitis
  • Venous thrombosis (“migratory thrombophlebitis”) –> secreted muscin acts like Tissue Factor + activates coagulaiton
18
Q

What are the characteristic of cstic tumours

What is the overall prognosis?

A

contain serouds or mucinous secreting cells

usually benign

19
Q

What are the characteristics of pancreatic endocrine neoplasms?

A

usually non-secretory

contain neuroendocrine markers e.g. chromogranin

behaviour difficult to predict (based on histology)

may be associated with the Multiple Endocrine Neoplasia (MEN) 1 syndrome

20
Q

What is chromogranin? What is it used for clinically?

A

Stains for neuroendocrine cells (very importnat to remember)

can also be used as plasma tumour marker

21
Q

What is the commonest kind of secretory neuroendocrine tumours?

What stain can be used to identify it?

A

Insulinomas
(derived from ß-cells)

stains positive for chromogranin

22
Q

What is the incidence of cholelithiasis?

A

Cholelihiasis = presence of gall stones
20% of adults in the westt

23
Q

What are the 2 most important sub-types of gallstones?

What are their macroscopic and radiographic appearances?

A
  1. 80% of gall stones: Cholesterol contain >50% of callstones (typcially single stones, mostly radiolucent)
  2. Pigmented –> contain calcium + unconjugated biliruin –> multiple, mosly radio-opaque
24
Q

What are the main complications of gall stones?

A
  • Cholecystiits (95% caused by galls stones)
  • Bile duct obstruction
  • Acute and chronic cholecystitis
  • Gall bladder cancer
  • Pancreatitis
25
Q

What are the main characterisitcs of chronic cholecystitis?

A
  • Chronic inflammation
  • Fibrosis (picture: thick wall)
  • Diverticula – Rokitansky-Aschoff sinuses (small black dots on wall)
  • 90% contain gall stones
26
Q

What is the main neoplasm of the gall bladder?

What is the main risk factor?

A

Adenocarcinoma
>90% associated with gall stones

Year 5 Path Histopathology (19 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions