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24 - Pancreatic and gall bladder pathology Flashcards

1
Q

What do I need to know

A
  1. acute and chronic pancreatitis
  2. pancreatic adenocarcinoma
  3. cholelithiasis
  4. acute and chronic cholecystitis
  5. GB adenocarcinoma (rare)
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2
Q

What are the symptoms of pancreas injury like and why?

A

They are non-specific and tend to present late in disease progression as it is a hidden organ

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3
Q

What cells make up the exocrine pancreas?

A

Acinar cells and ductal cells

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4
Q

Acinar cells contain …

A

Zymogen granules that contain inactive enzyme precursors for trypsin, chymotrypsin, elastase, nuclease, amylase, lipase (proenzymes)

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5
Q

What does damage to cells cause?

A

Damage to acinar cells causes release of pancreatic digestive enzymes

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6
Q

What activates the pancreatic enzymes?

A

Trypsin (activated form trypsinogen by enterkinases)

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7
Q

Why is inflammation of the pancreas usually increased compared to other organs?

A

Initial injury can cause damage to acinar cells causing release and premature activation of pancreatic enzymes that further damage the pancreas

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8
Q

How much of the pancreas function does the endocrine component make up and what does it consist of?

A
  • Islets of Langerhan
  • secretes insulin and glucagon
  • pathology is diabetes
  • only 10-20% of liver
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9
Q

Main pathologies of the pancreas

A
  • pancreatitis
  • cystic fibrosis
  • carcinoma
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10
Q

Are most cases of acute pancreatitis fatal?

A

60-70% are mild and most recover

30-40% are severe and 20-30% mortality rate

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11
Q

What are the 4 main mechanisms of pancreatitis?

A
  1. Metabolic
  2. Mechanical
  3. Vascular
  4. Infection
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12
Q

Metabolic mechanism of pancreatitis?

A

Alcohol

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13
Q

Mechanical pancreatitis?

A

Gallstone (cholelitiasis) and trauma

Obstruct and damage the pancreatic duct

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14
Q

Vascular pancreatitis?

A

Shock - low BP and organ perfusion, sepsis, trauma

Vasculitis

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15
Q

Infection pancreatitis?

A

Especially viral i.e. mumps

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16
Q

Most common causes of pancreatitis?

A

Alcohol and gallstones

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17
Q

What is the pathology of pancreatitis?

A
  • initial injury stimulus and body’s inflammatory response/cytokines damage pancreatic glands and acinar cells
  • release of pancreatic enzymes
  • autodigestion of pancreatic tissue
  • further increases inflammatory response, cytokine release and ongoing tissue damage
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18
Q

Consequence of pancreatic enzymes release?

A

Proteases - proteolytic destruction of acini, ducts, islets
Lipases - fat necrosis and pancreas and other sites
Elastases - damage BVs leading to interstitial bleeding and bleeding into glands
Cell Injury response - inflammation, oedema, ischaemia

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19
Q

What are the 2 main initial injury events that occur in the pancreas?

A
  1. Obstruction of the pancreatic duct

2. Direct injury to acinar cells

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20
Q
  1. Obstruction of the pancreatic duct
A
  • i.e. gall stones and ductal concretions
  • block enzyme (and HCO3-) release
  • pressure increase in pancreas and ducts
  • increase pressure
  • interstitial oedema and local inflammation
  • oedema compromises local blood flow leading to ischemia
  • fat necrosis as lipase active
  • damage to acinar cells and enz release
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21
Q
  1. Direct injury to acinar cells
A
  • alcohol, drugs, trauma, viruses, ischemia
  • inflammatory response
  • enzyme release
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22
Q

Clinical features of pancreatitis?

A

Non-specific

  1. Acute epigastric pain (LUQ)
  2. Nausea and vomitting (close to stomach)
  3. Fever and tachycardia - cytokine response
  4. Abdominal tenderness
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23
Q

How is pancreatitis diagnosed?

A
  • high WBC (generic to all inflammation)
  • MAIN: high serum amylase/lipase due to enzyme release into peripheral blood
  • CT scan (edema, pseudocysts, necrosis)
  • rarely laparotomy
  • epigastric tenderness
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24
Q

Management of acute pancreatitis?

A
  • conservative to rest pancreas to stop further enz secretion and further inflammation so it can start to heal
  • may include IV and NG suction to avoid stimulation of enzyme secretion
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25
Chronic pancreatitis definition
Repeated occurrences of pancreatic inflammation leading to chronic inflammation with damage and eventual loss of parenchymal tissue (pancreas functional cells) that is REPLACED by fibrous tissue
26
Most common cause of chronic pancreatitis?
Heavy alcohol intake (70-80% of cases)
27
Features of pancreas in chronic pancreatitis?
- Fibrotic and hard and calcification | - atrophy of exocrine acini while endocrine islets are spared
28
Clinical features of chronic pancreatitis?
- repeated attacks of abd pain often brought on by alcohol - if ongoing can get loss of exocrine function causing maldigestion and malabsorption - pseudocysts; NECROTIC pancreas surrounded by fibrosis - rarely get diabetes due to endocrine insufficiency
29
Diagnosis of chronic hepatitis?
Mainly via clinical suspicion | Can also include serum amylase but may not be elevated and CT
30
Pancreatic carcinoma
- usually adenoC - older (50+ 60-80) - poor prognosis due to anatomy/positioning as a hidden organ - males slightly > female - only 15-20% operable
31
What is the survival rate of pancreatic carcinoma at 5 years
less than 5%
32
What are the risk factors for pancreatic cancer
smoking, alcohol, diet/lifestyle/bmi, rare genetic diseases | not well associated risks
33
Where do most pancreatic cancers occur
- 60-70% in head - 10-15% tail - 5-19% body - 20% diffuse/throughout pancreas
34
Compare and contrast cancer in the head and body/tail
head - can invade ampulla causing biliary obstruction and jaundice - body and tail can remain silent until they present and by then large and disseminated/spread to nodes, adjacent organs, liver, bones so has poor prognosis
35
Does cancer in the head or body have poorer prognosis
Body/tail
36
Where do most pancreatic cancers occur
the head
37
What are clinical features of pancreatic cancer
- if in head and affecting ampulla then obstructive jaundice - pain - weight loss - pancreatitis - venous thrombosis
38
How is an unprovoked DVT related to pancreatic cancer
Pancreatic cancer is a risk factor for venous thrombosis. Therefore if someone presents with a sudden unprovoked thrombosis should investigate to see if there is an underlying pancreatic malignancy
39
How is diagnosis of pancreatic cancer made?
- usually made on imaging; CT or US followed by a biopsy of the tumour as guided by imaging
40
Endocrine tumours?
- rare - increase or decrease pancreatic tumours - insulinoma will secrete insulin and can result in hypoglycaemia - most are benign
41
Gallstone also called
Cholelithiasis
42
Is cholelithiasis common?
Yes. 10-20% of people have gallstones BUT 80% of these don't cause symptoms or problems or risk
43
What kind of gallstones are most?
Cholesterol stones
44
What do cholesterol stones contain
Crystalline cholesterol monohydrate
45
What are gallstones?
Saturated bile fluids that form crystals and stones
46
What are the less common type of gallstones, when do they usually occur and what are they made of
Pigement stones Made of bilirubin and calcium salts Usually occurs when there is abnormal amounts of breakdown of RBCs
47
Why do cholesterol stones occur
- are lifestyle related - bile becomes super-saturated with cholesterol - stasis favours crystal formation - if the crystals are then stasis in the GB for too long then stones are formed
48
Are gallstones more likely in women or men
WOMEN
49
Risk factors for gallstones?
- women and older people - estrogen i.e. the pill or pregnancy - obesity - rapid weight loss - GB stasis - family history - lifestyle disease
50
What is reason to believe that gallstones are lifestyle related
Gallstones are uncommon in developing and underdeveloped societies
51
What are the 2 major clinical consequences of gallstones
1. Cholecystitis (inflammation of the GB - acute/chronic) | 2. Biliary colic (due to choledocolithiasis and pain from continuing persistalsis trying to clear bile duct)
52
What are other clinical consequences as a result of cholecystitis and biliary colic
- cholangitis (inflammed bile duct - often due to bacteria in a closed off environment) - obstructive cholestasis > jaundice - pancreatitis (esp if blockage at ampulla)
53
Inflammation of GB
cholecystitis
54
Why do you normally see cholecystitis
Usually do not see without gallstones | Usually occurs due to obstruction at the neck of the GB or the cystic duct
55
Why do gallstones cause cholecystitis
- obstruction in neck or cystic duct - stasis of bile - FIRST this causes chemical irritation of the mucosa - secondary the stasis of bile and protection from outside world allows for bacterial infection
56
Clinical features of acute cholecystitis
- RUQ pain and tenderness post fatty meal as GB stimulated - non-specific inflam response/symptoms - neutrophil leucocytosis/increased WBC (non-specific) - if stone in CBD and inflam here then increased bilirubin, ALP, GGT - image GB via ultrasound
57
What does chronic cholecystitis result from?
Results from longterm association of gallstones and subsequent inflammation or may have a history of repeated acute cholecystitis
58
How does a chronically infammed GB present compared to an acutely inflammed GB
Long term inflammation causes it to be... - thickened walls - contracted - fibrotic and scarred - shrunken (OR may be enlarged or normal) An acutely inflamed GB will be red, inflamed, swollen/oedema, dilated BVs
59
Management of cholecystitis
Like in pancreas is mostly conservative trying to decrease activity - IV fluid, pain relief - to allow it to settle and cope with the inflam itself Possibly anti-biotics 25% require surgery but this is avoided as carries more risks when inflamed
60
What if long-term the inflammation doesn't settle?
Surgery - cholecystectomy | Quick recovery time as not open surgery
61
Choledocolithiasis
- stones in CBD - risk of obstructed ampulla and so pancreatic enzymes leading to pancreatitis - can lead to biliary obstruction - colicky abdominal pain - obstructive jaundice - cholangitis (inflam) i. e. symptoms due to obstruction, stasis of bile and accumulation of bacteria (infection)
62
Cancers of the biliary system?
1. Cancer of the GB 2. Cancer of the biliary ducts BOTH are rare and usually adenocarcinomas (glandular tissue)
63
Who do biliary system cancers occur in?
Older (70) females more than males usually late presentation with VERY poor prognosis (1% after 5 years) often invade the liver hence poor prognosis

Digestive (24 decks)

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