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Year 5 😊✌🏼 > Pancreas and Gallbladder Histopath > Flashcards

Pancreas and Gallbladder Histopath Flashcards

1
Q

Functions of the pancreas

A

Exocrine: production of digestive enzymes
Produces 2L a day of enzymic HCO3- rich fluid, stimulated by secretin and CCK. Exocrine pancreas is composed of ducts and acinar cells

Endocrine production of glucose-regulating hormones such as insulin and glucagon

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2
Q

Structure of the pancreas (micro)

A

acini made of acing and centroacinar cells secrete into intercalated ducts -> Pancreatic ducts

90% of pancreas is exocrine

Islets of Langerhans scattered through pancreas, made of alpha, beta, delta, epsilon and Pancreatic Polypeptide (PP) cells plus capillaries to secrete the hormones into

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3
Q

Neuroendocrine cells in the pancreas - where are they found?

A

Islets of Langerhans

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4
Q

Inflammatory diseases of the pancreas

A

acute pancreatitis
chronic pancreatitis
IgG4 related disease

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5
Q

acute pancreatitis - what causes the damage?

A

most damage caused by enzymes released by the pancreas

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

can cause acute abdomen

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6
Q

Causes of acute pancreatitis

A

Duct obstruction
- gall stones (50%)
- tumours
- trauma

Metabolic/toxic
-alcohol (33%)
- drugs e.g. thiazides
- hypercalcaemia
- hyperlipidaemia

Poor blood supply
- shock
- hypothermia

Infection/inflammation
- viruses e.g. mumps

Autoimmune
- IgG4 related disease

Idiopathic (15%)

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7
Q

Commonest cause of acute pancreatitis

A
  1. gallstones - 50%
  2. alcohol - 33%
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8
Q

Pathogenesis of acute pancreatitis

A
  1. Duct obstruction
    Gallstone stuck distal to where the common bile duct and pancreatic ducts join leads to:
    reflux of bile up the pancreatic duct followed by damage to acini and release of proenzymes which then become activated

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

  1. Direct acing injury (due to the causes other than obstruction and alcohol, e.g. infectious, inflammatory, shock etc)
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9
Q

Pattern of injury in acute pancreatitis

A

Periductal - necrosis of acinar cells near ducts (usually secondary to obstruction e.g. gallstones and alcohol)

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

Panlobular – develops from 1. and 2.

distribution of changes can give you hints on pathogenesis

Activated enzymes -> acinar necrosis -> enzyme release etc.
Ranges from stromal oedema, to haemorrhagic necrosis

e.g. Lipases -> fat necrosis (calcium ions bind to free fatty acids forming soaps which are seen as yellow-white foci)

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10
Q

Complications and prognosis of acute pancreatitis

A

pancreatic:
- pseudocyst
- abscess

systemic
- shock
- hypoglycaemia
- hypocalcaemia (because Ca combines with fatty acids to produce fatty necrosis)
- ARDS

Prognosis: overall mortality up to 50% for haemorrhagic pancreatitis

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11
Q

What is the prognosis of acute pancreatitis

A

overall mortality up to 50% for haaemorrhagic pancreatitis

if you only haave mild oedema you should be okay

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12
Q

Chronic pancreatitis - stats

A

relatively uncommon
mortality 3%/yr

relapsing, persistent, associated with acute pancreatitis in 50% cases

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13
Q

causes of chronic pancreatitis

A

Metabolic/toxic
- alcohol (80%)
- haemochromatosis (because iron can be deposited in the pancreas)

Duct obstruction
- gallstones
- abnormal pancreatic duct anatomy
- CF (chronic disease -> chronic pancreatitis)

Tumours

Idiopathic (autoimmune)

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14
Q

Pathogenesis of chronic pancreatitis

A

as for acute pancreatitis, e.g. acinar damage by digestive enzymes and necrosis

Chronic inflammation with parenchymal fibrosis and loss of parenchyma

Duct strictures with calcified stones with secondary dilatations

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15
Q

Complications of chronic pancretaitis

A

DM (late)
malabsorption
pseudocysts
?carcinoma of the pancreas (not sure yet, chicken and egg situation)

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16
Q

X-ray spot diagnosis of chronic pancreatitis

A

white foci in the pancreas area
calcifications

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17
Q

histopath chronic pancreatitis

A

fibrosis (pale pink) and loss of exocrine tissue parenchyma (acini disappear, the neuroendocrine tissue is still there mostly. sometimes this can make histopathologists question if this is chronic pancreatitis or a neuroendocrine tumour)

duct dilatation with thick secretions
calcification

lymphocytes

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18
Q

Pancreatic pseuodocyst

A
  • lined by fibrous tissue (not epithelial!!) - do not have a capsule
  • associated with acute and chronic pancreatitis
  • contain fluid rich in pancreatic enzymes or necrotic material
  • connect with pancreatic ducts
  • may resolve, compress adjacent structures, become infected or perforate
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19
Q

IgG 4 related disease

A

characterised by large number of IgG4 positive plasma cells

may involve the pancreas, gallbladder, bile ducts and any other part of the body…..
-> can cause autoimmune pancreatitis

histology shows: lots of plasma cells
IgG immunohistochemistry: brown stained cells

important ddx for e.g. pancreatic cancer and other pancreatic diseases

managed with steroids, just melts away

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20
Q

histology of IgG4 related diseases (pancreas)

A
  • ddx of pancreatic caancer
  • IgG4 positive plasma cells on histopath
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21
Q

How do you manage IgG4 related diseases?

A

responds well to steroids

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22
Q

categories of pancreatic tumours

A

carcinomas (ductal, acinar)

cystic neoplasms (serous cysstadenoma, mutinous cystic neoplasm)

pancreatic neuroendocrine tumours (islet cell tumours)

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23
Q

What are the comments cancer of the pancreas?

A

Ductal carcinomas (85%)

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24
Q

types of pancreatic carcinomas

A

ductal (85% of all pancreatic neoplasms)
acinar

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25
Q

types of cystic neoplasms in the pancraas

A

serous cyst adenoma
mutinous cystic neoplasm

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26
Q

5 yr survival of ductal carcinoma (pancreas) and stats

A

5%

increasingly common with age
2M : 1F

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27
Q

Risk factors for pancreatic carcinoma

A

smoking
BMI and dietary factors
chronic pancreatitis
diabetes

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28
Q

Pre-existing lesion in pancreas leading to pancreatic ductal carcinoma

A

Ductal carcinoma arises from dysplastic duc tal lesions:
- PanIN (pancreatic intraductal neoplasm)
- IMP (Intraductal Mucinous Papillary neoplasm )

Kras mutation in 95% cases

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29
Q

What mutation is common in Pre-existing lesion in pancreas leading to pancreatic ductal carcinoma

A

Kras mutation in 95%

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30
Q

Why do some pancreatic tumours present earlier based on their location?

A

tumours in the head present earlier than e.g. in the tail because they cause sooner obstructive symptoms

if in the tail etc. usually only present with mets to e.g. liver

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31
Q

Macroscopic ductal carcinoma of pancreas

A
  • Gritty and grey
  • Invades adjacent structures
  • Tumours in the head present earlier
  • hard because
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32
Q

Microscopic features of ductal carcinoma of pancreas

A

Adenocarcinomas:
mucin secreting glands set in desmoplastic stroma

-> secrete mucin
-> form glands
(this is true of any adenocarcinomas)

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33
Q

How do pancreatic carcinomas spread

A

direct -> duodenum, bile ducts
blood -> liver
lymphatics -> lymph nodes
serosa -> peritoneum

perineural spread if perineurial invasion (very characteristic)

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34
Q

areas of pancreatic carcinoma

A

Head 60%
body
tail
diffuse

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35
Q

complications of pancreatic ductal carcinoma

A
  • due to spread/metastases
  • chronic pancreatitis
  • venous thrombosis (migratory thrombophlebitis)
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36
Q

cystic tumours of pancreas

A
  • contain serous or mucin secreting epithelium (cf. ovarian tumours)
  • usually benign (mainly adenomas, rarely adenocarcinomas)
37
Q

Pancreatic endocrine neoplasms

A
  • usually non-secretory
  • contain neuroendocrine markers e.g. chromogranin
  • behaviour is difficult to predict
  • may be associated with MEN 1
38
Q

what is a neuroendocrine marker?

A

chromogranin (Can be detected In e.g. pancreatic neuroendocrine neoplasms)

39
Q

Commonest neuroendocrine tumour of pancreas

A

insulinoma (derived from beta cells)

stains for chromogranin

b-cells affected, secrete insulin

commonest type of secretory tumour

40
Q

How common are gallstones

A

20% adults in west have them

commoner in women
increasing age

common in native Americans

41
Q

What medications are RF for gallstones

A

oral contraceptives

42
Q

RFs for gall stones

A

increasing age
F >M
ethnic and geographic factors (e.g. native Americans)
hereditary (e.f. disorders of bile metabolism)
drugs (e.g. oral contraceptive)
acquired disorders (e.g. rapid weight loss)

43
Q

Different types of gallstones

A

cholesterol (must contain more than 50% cholesterol, mainly single and radiolucent)

pigment (contain calcium salts of unconjugated bilirubin, multiple, mostly radio-opaque, small)

44
Q

What gallstoness are not seen on xray?

A

cholesterol because hey are mostly single radiolucent

45
Q

What gallstoness are seen on xray and why?

A

pigment

because they contain calcium and are radio-opaque

usually small and multiple

46
Q

Complications of gall stones

A

bile duct obstruction
acute and chronic cholecystitis
gall bladder cancer
pancreatitis

47
Q

Acute cholecystitis

A

acute inflammation (neutrophil polymorphs)
90% associated with gallstones

48
Q

causes of acute no stones cholecystitis

A

salmonella, typhoid

49
Q

chronic cholecystitis

A

chronic inflammation (lymphocytes, neutrophils)
FIBROSIS - key for chronic
diverticula - Rokitasky-Aschoff sinuses
90% contain fall stones

thick gallbladder wall due to fibrosis

50
Q

What % of poeple with chronic cholecystitis have gallstones?

A

90%

51
Q

Rokitansky Aschoff sinuses

A
  • diverticula seen in chronic cholecystitis
  • mucosa pushed out into the wall by raised intralminal pressure
  • out pocketing of mucosa
52
Q

Gall bladder cancer

A

adenocarcinomas

90% associated with gallstones

53
Q

Which is the commonest type of pancreatic neoplasm?

A

ductal adenocarcinomas

54
Q

Which of the following most rarely causes chronic pancreatitis?

  1. alcohol
  2. gallstones
  3. CF
A

gallstones (are a very rare cause)

55
Q

The following are all complications of gall stone except

  1. acute cholecystitis
  2. gall bladder cancer
  3. haemolytic anaemia
  4. obstructive jaundice
A
  1. haemolytic anaemia is not a complication of gall stones

HA is itself a cause of gallstones

56
Q

Acute pancreatitis - how does duct obstruction cause damage?

A

Gallstones:
-> gallstone stuck distal to where the common bile and pancreatic ducts join
-> reflux of bile up the pancreatic duct
-> damage to the acini and release of proenzymes which become activated

Alcohol:
-> spasm/oedema of sphincter of Oddi
-> formation of a protein-rich pancreatic fluid which obstructs the pancreatic duct

57
Q

Name a neuroendocrine marker

A

chromogranin

58
Q

What is chromogranin?

A

A neuroendocrine marker

59
Q

Where is the pancreas located

A

in the retroperitoneum (secondarily retroperitoneal)

posterior to the stomach

between the duodenal curvature and the splenic hilum

60
Q

Gross anatomy of pancrease

A

head

uncinate process

neck

body

tail

61
Q

Where does the pancreas receive blood supply from and why?

A

from the coeliac trunk and its branches

because it is derived from the foregut

62
Q

Ducts in the pancreas

A

pancreatic duct begins in the tail

travels towards the head

then runs inferiorly

then joins the bile duct and forms the hepatopancreatic ampulla (Ampulla of Vater)

this enters the descending duodenum and the major duodenal papilla which is surrounded by the sphincter of Oddi

63
Q

What is the sphincter of Oddi

A

a collection of smooth muscles surrounding the ampulla of Vater

controls the secretion of bile and pancreatic fluid into the duodenum

64
Q

How many pancreatic ducts empty into the duodenum and how?

A

2

pancreatic duct after joining with the bike duct and forming the ampulla of Vater which empties into the descending duodenum via the major duodenal papilla

accessory pancreatic duct empties into the duodenum at the minor duodenal papilla, just above the major one

65
Q

hormones produced by the pancreas

A

glucagon
insulin
somatostatin

66
Q

vertebral level - pancreas

A

L1/L2

67
Q

Courvoisier sign

A

tumours in the pancreatic head often cause bile duct obstruction and can manifest with painless janudice

68
Q

How does the pancreas look like on histopath?

A

acini: small groups of cells making ‘circles’ that are pink on the inside and purple on the outside

islets of Langerhans: less dense

there may be big white bubbles which are adipocytes

69
Q

Where are secretin and CCK produced and what do they cause?

A

Secretin: produced by s-cells of the duodenum, controls gastric acid secretion and buffering with HCO3-
CCK: responsible for stimulating digestion of fat and protein. Made by I-cells in the duodenum. Causes release of digestive enzymes.

70
Q

Cells in the islets of largerhans and what they secrete

A

Alpha cells: glucagon increases blood glucose
Beta cells: insulin decreases blood glucose
Delta cells: somatostatin regulates the above cells
D1: a vasoactive peptide, stimulates the secretion of H20 into pancreatic system PP: pancreatic polypeptide, self regulates secretion activities

71
Q

What is metabolic syndrome and what are the components?

A

Collection of conditions that increase risk of IHD
● Fasting hyperglycaemia >6 mmol/l.
● BP >140/90
● Central obesity (>94cm in M, >80cm F)
● Dyslipidemia: Decreased HDL cholesterol <1mmol/l & Increased TGs >2mmol/l
● Microalbuminaemia

72
Q

diagnostic criteria for diabetes mellitus

A

Fasting plasma glucose >7 mmol/L
OR

random plasma glucose >11.1 mmol/L

OR

HBA1c >48 mmol/L.

73
Q

Scoring criteria for acute pancreatitis and when is it severe

A

GLASCOW scale

> or = 3 is severe

74
Q

causes of acute pancreatitis acronym

A

‘I GET SMASHED’:
Idiopathic (15%)
Gallstones (50%)
Ethanol (33%)
Trauma
Steroids
Mumps
Autoimmune
Scorpion venom
Hyperlipidaemia
ERCP
Drugs e.g. thiazides

75
Q

presentation of acute pancreatitis (incl blood markers)

A

severe epigastric (or central) pain radiating to back, relieved by sitting forward, vomiting prominent

Amylase only transiently increased. Serum lipase is more sensitive.

76
Q

acute pancreatitis histology

A

coagulative necrosis

77
Q

acute pancreatitis - causes of damage based on pattern of injury

A

Periductal → necrosis of acinar cells near ducts → obstructive causes.
Perilobular → necrosis at edge of lobules → ischaemic causes.
Panlobular → combination of both.

78
Q

fat necrosis in the pancreas - how does it occur?

A

lupines???? produce fat necrosis

calcium and fatty acid precipitates cause fat necrosis

“digestive enzymes react with visceral fat causing precipitation of calcium soaps (fat necrosis).” - meted

79
Q

lining of pancreatic pseudocyst

A

fibrous tissue (NOT epithelial)

therefore PSEUDOcyst

80
Q

What % alcoholics get acute pancreatitis?

A

5%

81
Q

Why is IgG4 related disease important in the context of the pancreas?

A

it is an important differential diagnosis for e.g. pancreatic cancer and can be managed simply with steroids which cause the disease to melt away in the pancreas

82
Q

what % of cancer deaths is due to ductal carcinoma of the pancreas?

A

5% of cancer deaths

83
Q

Why are pancreatic cancers hard?

A

because of desmostronal

84
Q

Insulinoma

A

derived form pancreatic beta cells
stains for chromogranin

commonest type of secretly tumour

85
Q

MEN - what are they and what types are theere

A

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 phaeochromocytoma), Pituitary adenoma.
  • MEN 2A- Parathyroid, Thyroid, Phaeochromocytoma
  • MEN 2B- Medullary Thyroid, Phaeochromocytoma, Acoustic Neuroma. Marfanoid
    phenotype
86
Q

What are the different types of gallbladder disease?

A

gallstones
inflammation
cancer

87
Q

Types of pancreatic malformations

A
  • Ectopic Pancreas – esp. stomach, small intestine.
  • Pancreas Divisum – failure of fusion of dorsal and ventral buds, increased risk of
    pancreatitis.
  • Annular pancreas – can present with duodenal obstruction approx. 1yo
88
Q

What are the different types of pancreatic neuroendocrine tumours

A
  • Functional – present with Sx related to hormone excess
    o Insulinoma – hypoglycaemic attacks(most common)
    o Gastrinoma – Zollinger-Ellison syndrome (high acid output):recurrent ulceration o Otherse.g.VIPoma–diarrhoea
    o Glucagonoma–necrolytic-migrating erythema
  • Non-functional – picked up incidentally on imaging or when grow large enough to produce symptoms of local disease or metastasis

Year 5 😊✌🏼 (53 decks)

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